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• W2002020135 abstract "Taurine modulates blood pressure and renal function. As the kidney plays a pivotal role in long-term control of arterial pressure, we tested the hypothesis that taurine-deficient rats display maladaptive renal and blood pressure responses to uninephrectomy. Control and taurine-deficient (i.e., β-alanine-treated) rats with either one or two remaining kidneys were fed diets containing basal or high (8%) NaCl diet. Urine osmolality was greater in the taurine-deficient than controls fed a normal NaCl diet; proteinuria and blood pressure were unaffected by uninephrectomy. Following 6 weeks on an 8% NaCl diet, the uninephrectomized (UNX) animals developed significant hypertension, which was more severe in the taurine-deficient group; baroreflex function was unaffected. However, the UNX taurine-deficient rats displayed impaired ability to dispose of an acute isotonic saline volume load before a switchover to a high NaCl diet. Nonetheless, a more protracted exposure (i.e., 14 weeks) to dietary NaCl excess eliminated the blood pressure differential between the two groups; at this stage, renal excretory responses to an acute saline volume load or to atrial natriuretic peptide were similar in the two groups. Nonetheless, hypertensive taurine-deficient rats displayed greater proteinuria, although both groups excreted proteins of similar molecular weights (∼15–66 kDa). Further, taurine-deficient kidney specimens displayed periarterial mononuclear cell infiltrates with strong immunoreactivity to the histiocyte marker CD68, suggestive of increased phagocytic activity. In conclusion, taurine deficiency modulates renal adaptation to combined uninephrectomy and dietary NaCl excess, resulting in an accelerated development of hypertension. Taurine modulates blood pressure and renal function. As the kidney plays a pivotal role in long-term control of arterial pressure, we tested the hypothesis that taurine-deficient rats display maladaptive renal and blood pressure responses to uninephrectomy. Control and taurine-deficient (i.e., β-alanine-treated) rats with either one or two remaining kidneys were fed diets containing basal or high (8%) NaCl diet. Urine osmolality was greater in the taurine-deficient than controls fed a normal NaCl diet; proteinuria and blood pressure were unaffected by uninephrectomy. Following 6 weeks on an 8% NaCl diet, the uninephrectomized (UNX) animals developed significant hypertension, which was more severe in the taurine-deficient group; baroreflex function was unaffected. However, the UNX taurine-deficient rats displayed impaired ability to dispose of an acute isotonic saline volume load before a switchover to a high NaCl diet. Nonetheless, a more protracted exposure (i.e., 14 weeks) to dietary NaCl excess eliminated the blood pressure differential between the two groups; at this stage, renal excretory responses to an acute saline volume load or to atrial natriuretic peptide were similar in the two groups. Nonetheless, hypertensive taurine-deficient rats displayed greater proteinuria, although both groups excreted proteins of similar molecular weights (∼15–66 kDa). Further, taurine-deficient kidney specimens displayed periarterial mononuclear cell infiltrates with strong immunoreactivity to the histiocyte marker CD68, suggestive of increased phagocytic activity. In conclusion, taurine deficiency modulates renal adaptation to combined uninephrectomy and dietary NaCl excess, resulting in an accelerated development of hypertension. The amino acid, taurine, serves as an important osmolyte in mammalian cells, including those of the kidney. Owing to this function, it has been suggested that the intracellular accumulation of taurine in renal tubule cells helps maintain intracellular osmolality and cell volume when exposed to the high extracellular ionic gradient of the medullary interstitium.1.Amiry-Moghaddam M. Nagelhus E. Ottersen O.P. Light and electronmicroscopic distribution of taurine, an organic osmolyte, in rat renal tubule cells.Kidney Int. 1994; 45: 10-22Abstract Full Text PDF PubMed Scopus (29) Google Scholar, 2.Kinne R.K. Boese S.H. Kinne-Saffran E. et al.Osmoregulation in the renal papilla: membranes, messengers and molecules.Kidney Int. 1996; 49: 1686-1689Abstract Full Text PDF PubMed Scopus (24) Google Scholar, 3.Nakanishi T. Takamitsu Y. Sugita M. Role of taurine in the kidney: osmoregulatory taurine accumulation in renal medulla.Adv Exp Med Biol. 1994; 359: 139-148Crossref PubMed Scopus (12) Google Scholar, 4.Pasantes-Morales H. Quesada O. Moran J. Taurine: an osmolyte in mammalian tissues.Adv Exp Med Biol. 1998; 442: 209-217Crossref PubMed Scopus (68) Google Scholar, 5.Trachtman H. Lu P. Sturman J.A. Immunohistochemical localization of taurine in rat renal tissue: studies in experimental disease states.J Histochem Cytochem. 1993; 41: 1209-1216Crossref PubMed Scopus (31) Google Scholar, 6.Uchida S. Nakanishi T. Kwon H.M. et al.Taurine behaves as an osmolyte in Madin–Darby canine kidney cells.J Clin Invest. 1991; 88: 656-662Crossref PubMed Scopus (102) Google Scholar Aside from its role in cell volume regulation, several lines of evidence also suggest that taurine modulates renal function and body fluid homeostasis through the release and renal actions of arginine vasopressin (AVP). First, taurine modulates AVP secretion from the supraoptic nucleus of the hypothalamus, raising the possibility for taurine-mediated modulation of body fluid status through a central mode of action.7.Hussy N. Deleuze C. Desarmenien M.G. Moos F.C. Osmotic regulation of neuronal activity: a new role for taurine and glial cells in hypothalamic neuroendocrine structure.Prog Neurobiol. 2000; 62: 113-134Crossref PubMed Scopus (167) Google Scholar Second, taurine-deficient rats display attenuated renal excretory responses to the administration of a hypotonic, but not a hypertonic, saline infusion.8.Mozaffari M.S. Warren B.K. Azuma J. Schaffer S.W. Renal excretory responses of taurine-depleted rats to hypotonic and hypertonic saline infusion.Amino Acids. 1998; 15: 109-116Crossref PubMed Scopus (5) Google Scholar Third, taurine-deficient rats display an elevated plasma AVP concentration in conjunction with increased baseline urine osmolality.9.Mozaffari M.S. Schaffer D. Taurine modulates arginine vasopressin-mediated regulation of renal function.J Cardiovasc Pharmacol. 2001; 37: 742-750Crossref PubMed Scopus (20) Google Scholar Fourth, following intravenous administration of a selective antagonist of the renal AVP receptor (e.g., V2 receptor), taurine-deficient rats display a more marked reduction in urine osmolality.9.Mozaffari M.S. Schaffer D. Taurine modulates arginine vasopressin-mediated regulation of renal function.J Cardiovasc Pharmacol. 2001; 37: 742-750Crossref PubMed Scopus (20) Google Scholar Yet, taurine deficiency reduces renal excretion of sodium and fluid following administration of an AVP receptor antagonist, suggesting that other factors beside the AVP system contribute to altered renal function in taurine-deficient animals.9.Mozaffari M.S. Schaffer D. Taurine modulates arginine vasopressin-mediated regulation of renal function.J Cardiovasc Pharmacol. 2001; 37: 742-750Crossref PubMed Scopus (20) Google Scholar Nonetheless, given the pivotal role of the kidney in chronic blood pressure regulation, it seemed likely that taurine deficiency might influence blood pressure through the modulation of renal function. Abnormal renal function is a feature of other conditions, such as spontaneous or salt-sensitive hypertension. When arterial pressure is reduced, the spontaneously hypertensive and the Dahl salt-sensitive rats excrete less sodium and fluid than their normotensive controls.10.Moreno C. Maier K.G. Hoagland K.M. et al.Abnormal pressure–natriuresis in hypertension: role of cytochrome P450 metabolites of arachidonic acid.Am J Hypertens. 2001; 14: 90S-97SCrossref PubMed Google Scholar, 11.Roman R.J. Cowley A.W. Abnormal pressure–diuresis–natriuresis response in spontaneously hypertensive rats.Am J Physiol. 1985; 248: F199-F205PubMed Google Scholar, 12.Roman R.J. Abnormal renal hemodynamics and pressure–natriuresis relationship in Dahl salt-sensitive rats.Am J Physiol. 1986; 251: F57-F65PubMed Google Scholar This suggests that a resetting of the pressure–diuresis–natriuresis mechanism occurs to re-establish fluid and sodium homeostasis. This important homeostatic mechanism becomes operative in the uninephrectomized (UNX) animal.13.Mozaffari M.S. Wyss J.M. Dietary NaCl-induced hypertension in uninephrectomized Wistar Kyoto rats: role of kidney function.J Cardiovasc Pharmacol. 1999; 33: 814-821Crossref PubMed Scopus (12) Google Scholar The removal of one kidney from a normotensive rat triggers compensatory mechanisms that enhance natriuresis and diuresis in the remaining kidney. As a result, the UNX rat remains normotensive when fed a basal NaCl diet. Nonetheless, when fed a high NaCl diet, the UNX rat develops a gradual and significant increase in blood pressure associated with an increased ability for diuresis and natriuresis.13.Mozaffari M.S. Wyss J.M. Dietary NaCl-induced hypertension in uninephrectomized Wistar Kyoto rats: role of kidney function.J Cardiovasc Pharmacol. 1999; 33: 814-821Crossref PubMed Scopus (12) Google Scholar Thus, the development of hypertension, in an otherwise normotensive rat, represents an adaptive or compensatory mechanism that allows the UNX animal to cope with an increased demand for diuresis and natriuresis imposed by the high NaCl diet. Nonetheless, protracted reliance on this adaptive mechanism has adverse consequences for the kidney, given the well-recognized impact of long-standing systemic hypertension on target organs.14.Cushman W.C. The burden of uncontrolled hypertension: morbidity and mortality associated with disease progression.J Clin Hypertens. 2003; 5: 14-22Crossref Scopus (67) Google Scholar, 15.Frohlich E.D. Target organ involvement in hypertension: a realistic promise of prevention and reversal.Med Clin N Am. 2004; 88: 209-221Abstract Full Text Full Text PDF PubMed Scopus (26) Google Scholar Interestingly, taurine treatment largely prevents age-dependent renal dysfunction of the UNX rat and ameliorates the deficit in renal excretory function of the hypertensive-glucose-intolerant rat.16.Mozaffari M.S. Schaffer S.W. Chronic taurine treatment ameliorates reduction in saline-induced diuresis and natriuresis.Kidney Int. 2002; 61: 1750-1759Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar, 17.Mozaffari M.S. Miyata N. Schaffer S.W. Effects of taurine and enalapril on kidney function of the hypertensive glucose-intolerant rat.Am J Hypertens. 2003; 16: 673-680Crossref PubMed Scopus (17) Google Scholar As taurine improves renal function, it is likely that taurine deficiency might adversely affect renal function of the UNX rat. Although the influence of taurine supplementation on the kidney and/or blood pressure has been investigated,16.Mozaffari M.S. Schaffer S.W. Chronic taurine treatment ameliorates reduction in saline-induced diuresis and natriuresis.Kidney Int. 2002; 61: 1750-1759Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar, 17.Mozaffari M.S. Miyata N. Schaffer S.W. Effects of taurine and enalapril on kidney function of the hypertensive glucose-intolerant rat.Am J Hypertens. 2003; 16: 673-680Crossref PubMed Scopus (17) Google Scholar, 18.Lee E.A. Seo J.Y. Jiang Z. et al.Reactive oxygen species mediate high glucose-induced plasminogen activator inhibitor-1 up-regulation in mesangial cells and in diabetic kidney.Kidney Int. 2005; 67: 1762-1771Abstract Full Text Full Text PDF PubMed Scopus (105) Google Scholar, 19.Michalk D.V. Hoffmann B. Minor T. Taurine reduces renal ischemia/reperfusion injury in the rat.Adv Exp Med Biol. 2003; 526: 49-56Crossref PubMed Scopus (18) Google Scholar, 20.Militante J.D. Lombardini J.B. Treatment of hypertension with oral taurine: experimental and clinical studies.Amino Acids. 2002; 23: 381-393Crossref PubMed Scopus (129) Google Scholar, 21.Mozaffari M.S. Azuma J. Patel C. Schaffer S.W. Renal excretory responses to saline load in the taurine-depleted and the taurine-supplemented rat.Biochem Pharmacol. 1997; 54: 619-624Crossref PubMed Scopus (15) Google Scholar, 22.Saad S.Y. Al-Rikabi A.C. Protection effects of taurine supplementation against cisplatin-induced nephrotoxicity in rats.Chemotherapy. 2002; 48: 42-48Crossref PubMed Scopus (95) Google Scholar, 23.Sato Y. Ando K. Fujita T. Role of sympathetic nervous system in hypotensive action of taurine in DOCA-salt rats.Hypertension. 1987; 9: 81-87Crossref PubMed Scopus (32) Google Scholar, 24.Trachtman H. Del Pizzo R. Futterweit S. et al.Taurine attenuates renal disease in chronic puromycin aminonucleoside nephropathy.Am J Physiol. 1992; 262: F117-F123PubMed Google Scholar to our knowledge, no information is available regarding the impact of endogenous taurine deficiency on renal function and blood pressure in animals with reduced renal mass. Therefore, we tested the hypothesis that the taurine-deficient rat displays maladaptive renal and blood pressure responses to the loss of one kidney and/or dietary NaCl excess. The results of protocol I (Figure 1) show that despite differences in fluid intake and urine excretion, the ratio of urine output to fluid intake remained similar in the control and taurine-deficient groups (Figure 2a–c). Nonetheless, urine osmolality was greater for the taurine-deficient, two-kidney rat than the control rat fed a basal NaCl diet (Figure 2d), suggesting altered regulation of urine concentrating ability.Figure 2Urine samples (48-h; protocol I) were collected from taurine-deficient and control animals for assessment of (a) cumulative fluid intake, (b) cumulative urine excretion, (c) ratio of urine output to fluid intake, and (d) urine osmolality. Data are means±s.e.m. of 4 rats/group. *P<0.05 compared to the control group.View Large Image Figure ViewerDownload (PPT) We then examined whether taurine deficiency affects the function of the stressed kidney undergoing compensatory overgrowth in response to uninephrectomy (protocol II, Figure 1; Figures 3, 4, 5 and 6). The taurine-deficient group, fed the normal NaCl diet, displayed a slight reduction in body weight after 3 weeks of uninephrectomy (250±7 vs 273±3 g; P<0.05). At the conclusion of the 11-week study (i.e., 6 weeks after the high NaCl diet), body weight was similar in the taurine-deficient and control groups (316±6 vs 321±4 g). The weight of the right kidney was unaffected by 2 weeks of β-alanine treatment (0.90±0.01 vs 0.90±0.04 g). At the conclusion of the study, the weight of the remaining left kidney was 1.80±0.05 g in the control group and 1.80±0.01 g in the taurine-deficient group. Thus, the remaining left kidney experienced a significant increase in weight post-uninephrectomy (i.e., 2–11 weeks), an effect owing to the combination of compensatory growth, high NaCl diet, development of hypertension, and aging.Figure 4Line graphs showing the effect of uninephrectomy alone and in combination with dietary NaCl excess on (a) daily fluid intake, (b) sodium excretion, (c) urine excretion, (d) potassium excretion, (e) urine osmolality, and (f) protein excretion in taurine-deficient and control rats. Data are means±s.e.m. of four control and five taurine-deficient rats. *P<0.05 compared to the other group at the same time.View Large Image Figure ViewerDownload (PPT)Figure 5The taurine-deficient rats developed a more exaggerated increase in mean arterial pressure, systolic pressure, and diastolic pressure than their control counterparts. Data are means±s.e.m. of four control and five taurine-deficient rats. *P<0.05 compared to the control group.View Large Image Figure ViewerDownload (PPT)Figure 6Bar graphs showing changes in (a) mean arterial pressure (MAP) and (b) heart rate of hypertensive control and hypertensive taurine-deficient (TD) rats in response to the intravenous administration of either phenylephrine or sodium nitroprusside. Data are means±s.e.m. of four control and five taurine-deficient rats.View Large Image Figure ViewerDownload (PPT) Figure 3 shows that 2 weeks of β-alanine treatment markedly reduced the taurine content of the right kidney. β-Alanine treatment was equally effective (on a percentage basis) in reducing taurine content in the right kidney before uninephrectomy and the left kidney following the combination of uninephrectomy and the high salt diet; myocardial taurine content was also reduced by β-alanine treatment (Figure 3). The slight, albeit significant, increase in taurine content of the remaining left kidney was related to the high salt diet, as rats with two intact kidneys showed a significant elevation in renal taurine content when fed a high NaCl diet for 2 weeks (12.8±0.6 vs 10.9±0.5 μmol/g wet wt., n=5 rats/group; P<0.05). Blood pressure and heart rate were unaffected in rats retaining two kidneys and fed a high NaCl diet (data not shown). The daily water intake (23.3±0.6 vs 27.5±0.9 ml) and excretion of fluid (11.6±0.4 vs 15.1±1.1 ml), sodium (0.9±0.05 vs 1.2±0.0 mEq) and potassium (4.2±0.2 vs 5.1±.2 mEq) tended to be lower in the two-kidney taurine-deficient rat than in the control rat fed the normal NaCl diet (e.g., day 4 values; Figure 4a–d). Following uninephrectomy, both groups excreted similar amounts of fluid and electrolytes over a 24-h period; the excretion values were similar to those achieved earlier with rats retaining two intact kidneys (Figure 4b–d). As expected, when the animals were switched to the high NaCl diet, daily intake of fluid was markedly increased (Figure 4a). Associated with the elevated intake of fluid and sodium, there was a marked increase in daily fluid and sodium excretion. However, potassium excretion was largely unaffected by the switch to the high NaCl diet (Figure 4a–d). A noted feature of the taurine-deficient rat with either one or two intact kidneys was the increase in urine osmolality (Figures 2d and 4e). When the UNX animals were switched to a high NaCl diet, both groups showed a marked decline in urine osmolality. However, the taurine-deficient group showed a large enough reduction in urine osmolality to eliminate the differential that existed between the two groups during consumption of the basal NaCl diet (Figure 4e). Daily protein excretion of rats fed the normal NaCl diet was similar in the taurine-deficient and the control groups, irrespective of the number of intact kidneys. Following the switchover to the high NaCl diet, both UNX groups displayed significant increases in proteinuria. Taurine deficiency did not affect daily protein excretion following 6 weeks on high NaCl diet (Figure 4f). Mean arterial pressure (113±7 vs 112±4 mm Hg; tail cuff) and heart rate (395±24 vs 376±13 beats/min) were similar in the two-kidney control and taurine-deficient groups fed the normal NaCl diet. Three weeks after uninephrectomy, mean arterial pressure (105±4 vs 113± 3 mm Hg) and heart rate (367±21 vs 364±20 beats/min) remained similar in the two groups; both groups consumed the normal NaCl diet during this time. Thus, neither taurine deficiency nor uninephrectomy alone significantly affected blood pressure or heart rate. However, switching the UNX animals to the high NaCl diet resulted in a gradual increase in blood pressure in both groups. Yet, as shown in Figure 5, the taurine-deficient group developed a more exaggerated increase in blood pressure than the control group. It is noteworthy that loss of one kidney at about 10, in contrast to 4 weeks of age, results in a more accelerated decline in diuresis and natriuresis.25.Mozaffari M.S. Patel C. Ballas C. Schaffer S.W. Effects of chromium picolinate treatment in uninephrectomized rat.Metab Clin Exp. 2005; 54: 1243-1249Abstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar This likely underlies the earlier, more robust, increase in blood pressure in this study than when uninephrectomy is performed at 4 weeks of age.13.Mozaffari M.S. Wyss J.M. Dietary NaCl-induced hypertension in uninephrectomized Wistar Kyoto rats: role of kidney function.J Cardiovasc Pharmacol. 1999; 33: 814-821Crossref PubMed Scopus (12) Google Scholar Interestingly, however, both groups displayed similar changes in mean arterial pressure and heart rate to escalating doses of either phenylephrine or sodium nitroprusside (Figure 6). Thus, under these conditions, it is unlikely that taurine deficiency causes a dysfunctional baroreflex mechanism. We reasoned that development of exaggerated blood pressure in response to dietary NaCl excess in the UNX taurine-deficient rat may relate to abnormal adaptation of the animal to the need for greater diuresis and natriuresis. Although daily fluid and sodium excretion was not affected by taurine deficiency in the UNX rat (Figure 4b–c), we conjectured that a deficit in renal excretory function would be present in the UNX taurine-deficient rat fed the basal NaCl diet (i.e., before development of NaCl-induced hypertension). We further hypothesized that the functional deficit contributed to the greater rise in blood pressure. Moreover, the deficit could be unmasked following maneuvers (e.g., volume expansion) requiring enhanced diuresis and natriuresis. In comparison to the UNX control rat, the UNX taurine-deficient rat exhibited a reduction in diuresis and natriuresis following a 5% isotonic saline volume load (Figure 7); these responses were determined 3 weeks post-uninephrectomy whereas the animals were fed the basal NaCl diet (protocol III, Figure 1). As glomerular function was only slightly reduced by taurine deficiency (Figure 7d) whereas the fractional excretions of fluid and sodium were significantly reduced in the taurine-deficient rat, the reduction in saline volume-induced diuresis and natriuresis is primarily related to enhanced tubular reabsorption of fluid and sodium (Figure 7e–f). Similar results were obtained with control (n=3) and taurine-deficient (n=4) animals infused with a 10% isotonic saline load (intravenounsly); 90 min after initiation of infusion, control animals excreted 18–24%, whereas taurine-deficient animals excreted 11–17% of the administered sodium (P=0.0502) and fluid (P<0.05) loads. The effect of taurine deficiency on blood pressure could relate to the acceleration and/or exacerbation of NaCl-induced hypertension. Therefore, in protocol IV (Figure 1), additional groups of UNX control and taurine-deficient rats were monitored for 14 weeks after initiation of dietary NaCl excess. Figure 8a shows that taurine deficiency accelerated NaCl-induced hypertension, with blood pressure being higher in the taurine-deficient rats during the initial 8 weeks of dietary NaCl excess. However, both groups displayed similar blood pressure values with prolonged high NaCl feeding (Figure 8a). Neither heart rate (Figure 8b), body weight (376±7 vs 358±9 g), nor kidney weight (2.1±0.1 vs 2.1±0.1 g) were significantly affected by superimposing taurine deficiency on hypertension. As expected, taurine content of the remaining left kidney was lower in the hypertensive taurine-deficient rats than the hypertensive control group (≈46%; P<0.05). Interestingly, the hypertensive taurine-deficient rats exhibited greater (≈27%) proteinuria than their hypertensive control counterparts (Figure 8c; P<0.05), although both groups excreted proteins of similar molecular weights (∼15–66 kDa; Figure 8d). Interestingly, urine samples of hypertensive rats displayed a protein band of similar molecular weight to that of bovine serum albumin, a feature not seen with urine samples from age- and strain-matched normotensive rats (Figure 8d). In order to determine whether impaired renal excretory function is a feature of the taurine-deficient rat during the ‘established’ phase of NaCl-induced hypertension (i.e., protocol IV), renal excretory responses to an acute isotonic saline volume expansion (5% of body weight) were determined. After an overnight rest, renal and hemodynamic responses were also determined following intravenous administration of atrial natriuretic peptide (ANP); ANP is normally released following central hypervolemia and exerts prominent effects on the kidney.16.Mozaffari M.S. Schaffer S.W. Chronic taurine treatment ameliorates reduction in saline-induced diuresis and natriuresis.Kidney Int. 2002; 61: 1750-1759Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar As shown in Figure 9, diuretic and natriuretic responses to either an isotonic saline volume expansion or administration of atrial natriuretic peptide were similar in the hypertensive control and hypertensive taurine-deficient rats. Baseline values for glomerular filtration rate and fractional excretion of fluid and sodium were similar in the two groups; both groups displayed similar changes in these parameters during administration of either an isotonic saline volume load or atrial natriuretic peptide (data not shown). While blood pressure was not significantly affected by administration of the 5% saline volume load, it decreased following ANP administration with the effect greater in the taurine-deficient than in the control hypertensive rats (14 vs 7 mm Hg; P<0.05 for the former group). In light of the greater proteinuria in the hypertensive taurine-deficient group, renal tissues were processed for light microscopy. Histological examination of the kidneys revealed generally similar glomerular, tubular and vascular architecture, and foci of tubular dilatation with colloidal casts for the two groups (Figure 10a and b hematoxylin–eosin); periodic acid Schiff-stained tissue sections are not shown. However, the most distinguishing feature between the two groups was the presence of periarterial mononuclear cell infiltrates in taurine-deficient kidneys (Figure 10b–d). These infiltrates were composed of polyhedral cells, which exhibited convoluted vesicular nuclei surrounded by eosinophilic cytoplasm. These cells were interpreted as histiocytes and reacted positively to the histiocytic marker CD68 (Figure 10d), whereas the hypertensive kidneys did not show these mononuclear cell infiltrates (Figure 10 panel d, inset). No immunoreactivity was detected against LCA or CD21, markers of lymphocytes or dendritic cells, respectively (data not shown). A novel finding of this study is that hypertension is accelerated in the UNX, taurine-deficient rat fed a high NaCl diet. This effect of taurine deficiency is not associated with impairment in baroreflex function. Rather, the UNX, taurine-deficient rat manifests an impaired ability to dispose of an acute saline volume load during periods of normal NaCl feeding. During high NaCl feeding, this renal deficit predisposes the animal to an accelerated rise in blood pressure, with the hypertension being a compensatory coping mechanism that allows for enhanced diuresis and natriuresis. Interestingly, however, with a more protracted period of high NaCl consumption (i.e., 6 vs 14 weeks), blood pressure further rises in the UNX control causing the differential in blood pressure between the taurine-deficient and control rats to be eliminated. Renal excretory responses to the administration of either a saline volume expansion or to ANP were similar in the two groups during this ‘established’ phase of hypertension (i.e., protocol IV). Despite similar blood pressure values, during the ‘established’ phase, the hypertensive taurine-deficient rats displayed greater proteinuria, suggesting a differential susceptibility to the adverse effect of high blood pressure. Taken together, the results indicate that taurine deficiency affects renal adaptation to the stresses of reduced mass and elevated dietary NaCl, resulting in accelerated development of hypertension. We have previously shown that augmented sympathetic nervous system activity contributes to the development of hypertension in the UNX rat fed a high NaCl diet.26.Mozaffari M.S. Patel C. Warren B.K. Schaffer S.W. NaCl-induced hypertensive rat model of non-insulin-dependent diabetes: role of sympathetic modulation.Am J Hypertens. 2000; 13: 540-546Crossref PubMed Scopus (7) Google Scholar Taurine is reported to exert a sympatholytic effect and affect vascular reactivity.23.Sato Y. Ando K. Fujita T. Role of sympathetic nervous system in hypotensive action of taurine in DOCA-salt rats.Hypertension. 1987; 9: 81-87Crossref PubMed Scopus (32) Google Scholar, 27.Abebe W. Mozaffari M.S. Effect of taurine deficiency on adenosine receptor-mediated relaxation of the rat aorta.Vasc Pharmacol. 2003; 40: 219-228Crossref PubMed Scopus (15) Google Scholar, 28.Abebe W. Mozaffari M.S. Taurine depletion alters vascular reactivity in rats.Can J Physiol Pharmacol. 2003; 81: 903-909Crossref PubMed Scopus (24) Google Scholar, 29.Abebe W. Mozaffari M.S. Effects of chronic taurine treatment on reactivity of the rat aorta.Amino Acids. 2000; 19: 615-623Crossref PubMed Scopus (33) Google Scholar It is likely that taurine deficiency provides a more permissive environment for the development of accelerated hypertension because taurine's sympatholytic effect should be attenuated and the vasoconstrictor responses enhanced. Sympathoexcitation and changes in vascular reactivity also mediate the hypertensinogenic effect of dietary NaCl excess in other animal models.30.Adeagbo A.S. Zhang X. Patel D. et al.Cyclo-oxygenase-2, endothelium and aortic reactivity during deoxycorticosterone acetate salt-induced hypertension.J Hypertens. 2005; 23: 1025-1036Crossref PubMed Scopus (38) Google Scholar, 31" @default.
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• W2002020135 title "Accelerated NaCl-induced hypertension in taurine-deficient rat: Role of renal function" @default.
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