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• W2045659493 abstract "It is clear that a large number of neurotransmitters and neuromodulators act at G-protein coupled receptors (GPCR) influencing the activity of presympathetic neurons in the rostral ventrolateral medulla (RVLM). The role of some of these GPCR play in the RVLM on the tonic and reflex control of arterial pressure has been investigated. For example, activation of muscarinic receptors increases arterial pressure and enhances the baroreceptor reflex whilst attenuating and inhibiting the chemoreceptor and somatosympathetic reflexes respectively [1] whereas activation of somatostatin receptors evokes profound hypotension and attenuates the somatosympathetic and chemoreceptor reflexes but does not alter sympathetic baroreflex function [2]. The role of downstream signaling cascades or effectors in the RVLM is poorly explored and provides another strategy by which to explore the role of these neurons in the regulation of arterial pressure. Here we explore the role of two effectors: cAMP and voltage gated calcium channels. In urethane anesthetized, paralysed and artificially ventilated rats the effects of cAMP analogues, which activate or inhibit PKA or EPAC, and calcium channel blockers evoke were determined in normotensive and hypertensive rat strains: Sprague Dawley, Wistar–Kyoto and spontaneously hypertensive rats. Microinjections were made into the RVLM or administered intrathecally and arterial pressure, heart rate and splanchnic sympathetic nerve activity were measured. In the RVLM, Sp-cAMPs (an activator of PKA) evoked a large increase in arterial pressure (55±13 mmHg, 5 nmol, n=4) and sympathetic nerve activity (115±19%) and facilitated somatosympathetic reflex function whereas inhibition of PKA (Rp-cAMPs) also evoked an increase in arterial pressure (33±3 mmHg, n=4) and SNA (40±5%). In the spinal cord, activation of PKA does not evoke a response on the parameters indicated. Whether or not these effects are altered under hypertensive conditions is currently being investigated. Previously, we have demonstrated that blockade in the RVLM of a nickel sensitive conductance, presumably a T-type channel, evoked a large inhibition in sympathetic activity although reflex function was unaffected in normotensive animals [3]. In hypertensive animals (SHR), the effects of similar injections of 50 mM nickel chloride evoked a profound increase in SNA (53±4%, n=4) and arterial pressure (30±6 mmHg). We are currently exploring the role of T-type calcium channels in controlling the sympathetic outflow in the spinal cord. These studies indicate that a cAMP dependent pathway is tonically active in the RVLM but not in the spinal cord under normotensive conditions. This pathway may participate in setting the level of arterial pressure. Furthermore, T-type channels are tonically active in the RVLM in normotensive conditions but under hypertensive conditions the function of these channels change. Investigating the role signaling transduction proteins and channels play is a fruitful strategy for elucidating function of central regions participating in cardiovascular control." @default.
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• W2045659493 date "2009-08-01" @default.
• W2045659493 modified "2023-09-27" @default.
• W2045659493 title "P7.8 Role of cAMP dependent effectors and voltage gated calcium channels in the rat rostral ventrolateral medulla and in the spinal cord in the tonic and reflex control of arterial pressure in hypertension and normotension" @default.
• W2045659493 doi "https://doi.org/10.1016/j.autneu.2009.05.211" @default.
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