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Renal nerve stimulation

Renal nerve stimulation Afferent-tefferent arteriolar constriction [245]... [Pg.189]

Chen J, Fleming JT Juxtamedullary afferent and efferent arterioles constrict to renal nerve stimulation. Kidney Int 44 684-691, 1993... [Pg.215]

Renal nerve stimulation Afferent -i- efferent arteriolar constriction [311]... [Pg.100]

Maneuvers that increase renal nerve activity cause stimulation of renin secretion, whereas renal denervation results in suppression of renin secretion. Norepinephrine stimulates renin secretion by a direct action on the juxtaglomerular cells. In humans, this effect is mediated by 13 i adrenoceptors. [Pg.375]

Miller RJ (1998) Presynaptic receptors. Annu Rev Pharmacol Toxicol 38 201-27 Modin A, Pernow J, Lundberg JM (1994) Repeated renal and splenic sympathetic nerve stimulation in anaesthetized pigs. J Auton Nerv Syst 49 123-34 Moran TD, Colmers WF, Smith PA (2004) Opioid-like actions of neuropeptide Y in rat substantia gelatinosa Y1 suppression of inhibition and Y2 suppression of excitation. J Neurophysiol 92 3266-75... [Pg.432]

Lang RJ, Zhang Y, Exintaris B, Vogalis F (1995) Effects of nerve stimulation on the spontaneous action potentials recorded in the proximal renal pelvis of the guinea pig. Urol Res 23 343-350... [Pg.136]

Modin, A., Pernow, J. Lundberg, J.M. (1993a) Repeated renal and splenic sympathetic nerve stimulation in anaesthetized pigs maintained overflow of neuropeptide Y in controls but not after reserpine. J. Auton. Nerv. Syst. 49, 123-134. [Pg.52]

Dopamine can exert pronounced cardiovascular and renal effects through the activation of both Dj- and Dz-receptor subtypes. Stimulation of the Dj-receptor, which is present on blood vessels and certain other peripheral sites, will result in vasodilation, natriuresis, and diuresis. Dz-receptors are found on ganglia, on sympathetic nerve terminals, on the adrenal cortex, and within the cardiovascular centers of the CNS their activation produces hypotension, bradycardia, and regional vasodilation (e.g., renal vasodilation). The kidney appears to be a particularly rich source for endogenous dopamine in the periphery. [Pg.104]

Pigott TA, HillJL, Gardy TA, et al A comparison of the behavioral effects of oral versus intravenous mCPP administration in OCD patients and the effect of metergoline prior to i.v. mCPP [see comments]. Biol Psychiatry 33 3-14, 1993 Pilowsky R, West M, Chalmers J Renal sympathetic nerve responses to stimulation, inhibition and destruction of the ventrolateral medulla in the rabbit. Neurosci Lett 60 51-55, 1985... [Pg.719]

Dopamine is an endogenous catecholamine and an immediate precursor of adrenaline and noradrenaline. At low doses it stimulates vascular DAI dopaminergic receptors, especially those in renal, mesenteric and coronary vessels. As the dose increases it progressively stimulates 31 and al adrenoceptors. Thus, depending on the dose it may act as a renal vasodilator, a myocardial inotrope, or a peripheral vasoconstrictor. Dopamine also causes release of noradrenaline from autonomic nerve endings (DA2 receptors). [Pg.153]

Beta Postsynaptic effector cells, especially heart, lipocytes, brain presynaptic adrenergic and cholinergic nerve terminals, juxtaglomerular apparatus of renal tubules, ciliary body epithelium Stimulation of adenylyl cyclase, increased cAMP... [Pg.118]

Dopamine has been used for several decades for the treatment of human patients with oliguric ARF (Denton et al 1996, Dishart Kellum 2000). A constant low-dose i.v. infusion (0.5 to 3.0(jLg/ kg/min) produces a dose-dependent increase in the RBF and increases the excretion of sodium and water. Some studies have also reported increases in the GFR but this response is less consistent. A dose-dependent increase in the RBF has also been documented in normal horses (Trim et al 1989). Low doses of dopamine augment the RBF primarily by inducing renal arteriolar vasodilatation by stimulating dopamine D receptors in the intrarenal blood vessels. This effect is typically greater in afferent than in efferent glomemlar arterioles and is the mechanism by which dopamine may also promote an increase in the GFR. A secondary role is the stimulation of D2 receptors on presynaptic sympathetic nerve terminals, which inhibits norepinephrine release. Intermediate doses... [Pg.157]

Myoepithelia Basket-shaped, mononuclear cells surrounding the acini of exocrine glands have cytoplasmic fibrils resembling smooth muscle derived from ectoderm rather than mesoderm. Contraction stimulated by hormones (e.g., oxytocin) and presumably by autonomic nerves may have noncontractile functions such as pressure transduction in the renal cortex. Contraction to expel contents of exocrine glands (salivary, sweat, mammary) form the dilator muscle of the iris may be the pressure transducers in juxtaglomerular cells. [Pg.455]

Both presynaptic and postsynaptic adrenoceptors are present in the vasculature. Postsynaptic a - and 2-receptors mediate vasoconstriction, whereas postsynaptic /32-receptors induce vasodilation. Presynaptic a2-receptors inhibit norepinephrine release in the vasculature as well. Presynaptic /3i-adrenoceptors promote neurotransmitter release. Stimulation of peripheral DAj -receptors produces renal, coronary, and mesenteric vasodilation and a natriuretic response. Stimnlation of DA2-receptors inhibits norepinephrine release from sympathetic nerve endings and prolactin release and may in-dnce nansea and vomiting. DAj- and DA2-receptor stimulation also... [Pg.466]

Corticosteroids, CSA, TAC, and impaired kidney graft function may cause post-transplant hypertension. The primary mechanism of CI-associated hypertension in heart transplant recipients may be related to the Cl-induced stimulation of intact renal sympathetic nerves and the absence of reflex cardiac inhibition of the sympathetic nervous system, but a number of other mechanisms, including decreased prostacyclin and nitric oxide production, also have been proposed. " In addition to the propensity to cause peripheral vasoconstriction, CIs promote sodium retention, resulting in extracellular fluid volume expansion. TAC appears to have less potential to induce hypertension following transplantation than CSA. Most classes of antihypertensive medications effectively reduce blood pressure in transplant patients (see Chap. 13). ... [Pg.1636]


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