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• W1998879778 abstract "Abstract We are now in a position to attempt a synthesis of the evidence for the participation of hepatorenal vasotropic factors in experimental renal hypertension. Shortly after the partial constriction of the renal artery by a Goldblatt clamp, significant amounts of VEM appear first in the renal vein blood and then in the peripheral circulation. The mechanism responsible for this shift in humoral equilibrium appears to be a specific alteration in renal metabolism as a result of which VEM is formed aerobically as well as anaerobically. This situation is indicative of a breakdown of the normal intracellular homeostatic mechanism by which in vitro VEM formation can be regulated by variations in oxygen tension. Acute in uivo and in vitro experiments suggest that this derangement is brought about by the period of hypoxia attendant upon the initial reduction of renal blood flow which follows application of the clamp. This defect in the renal VEM mechanism of the clamped kidney persists throughout the syndrome. Nevertheless, a preponderance of humoral VEM prevails only during the period of rising blood pressure. When the blood pressure has been stabilized at hypertensive levels, presumably with the restoration of an adequate renal blood flow, the blood again becomes neutral. This neutrality is due to the appearance in the blood stream of increasing amounts of VDM which eventually reach a concentration adequate to neutralize the heightened concentration of VEM. The neutral state therefore represents the establishment of a new equilibrium between VEM and VDM at greatly augmented concentrations of both factors. A similar situation exists in the blood of patients with essential hypertension. The reasons for the persistence of the hypertensive state when the blood has again become neutral remains a matter for further study. The persistence of this defect in the renal VEM mechanism in dogs with one kidney clamped and the other intact and in whom the blood pressure has returned to normal, suggests that the unclamped hypertrophied kidney is inactivating the excess VEM which is continuously elaborated by the clamped kidney. A relation of the above phenomena to the adrenal cortex was brought out by experiments which showed that kidneys from adrenalectomized animals could no longer form VEM in vitro . Desoxycorticosterone, but not NaCl, restores this mechanism to the kidney of the adrenalectomized animal." @default.
• W1998879778 created "2016-06-24" @default.
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• W1998879778 date "1948-01-01" @default.
• W1998879778 modified "2023-09-26" @default.
• W1998879778 title "Participation of hepatorenal vasotropic factors in experimental renal hypertension" @default.
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• W1998879778 doi "https://doi.org/10.1016/0002-9343(48)90378-7" @default.
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