Sympathetic nervous system renal effects

Conflicting results have been published with regards to the effects of renal denervation on hypertension. Further studies are needed to clarify these relationships and the mechanisms of the renal sympathetic nervous system in hypertension. 

The randomized controlled clinical trials performed by Freis and his colleagues at the Veterans Administration Hospitals have provided some of the first solid evidence that moderate permanent hypertension has an improved prognosis when actively treated by sodium depletion (hydrochlorothiazide), by interruption of the sympathetic nervous system (reserpine) and with a vasodilator (hydralazine) (262). In parallel, the beneficial effects of this triple therapy were demonstrated in spontaneously hypertensive rats by the spectacular prevention and cure of their cardiac, vascular, and renal lesions (263). 

Local blood vessel effects (vascular smooth muscle hypertrophy) Exaggerated activity of the sympathetic nervous system Defect in renal excretion of sodium... 

The cardiac and renal hemodynamic effects of debrisoquin sulfate have been studied in hypertensive patients and found to be similar to those observed with guanethidine and the ganglionic blocking agents. Lowered blood pressure associated with reduced cardiac output and renal blood flow are apparently characteristic of the hemodynamic pattern of inhibition of the peripheral sympathetic nervous system."... 

Effects of cannabinoids on the sympathetic nervous system have been studied in isolated tissues and in pithed animals (Table 4). Sympathetic neurons were usually activated by electrical stimulation. Activation of CBi receptors led to inhibition of noradrenaline and/or ATP release and, consequently, to inhibition of the effector responses in the heart, in mesenteric and renal blood vessels and in the vas deferens. Figure 5A shows that cannabinoids inhibit sympathetic neuroeffector transmission in the heart. Sympathetically mediated vasoconstriction was inhibited in many tissues of pithed rats and rabbits. Sympathetic tone is depressed during long-term A -tetrahydrocannabinol administration in humans the presynaptic inhibitory effect of cannabinoids on sympathetic axon endings maybe the basis of this effect. 

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). ... 

Cardiovascular System Desflurane lowers blood pressure—primarily by decreasing systemic vascular resistance—and has a modest negative inotropic effect. Thus, cardiac output is preserved, as is perfusion of major organ beds (e.g., splanchnic, renal, cerebral, and coronary). Marked increases in heart rate often occur during induction of desflurane anesthesia and with abrupt increases in the delivered concentration of desflurane this results from desflurane-induced stimulation of the sympathetic nervous system. The hypotensive effects of desflurane do not wane with increasing duration of administration. 

Hydralazine (apresoline) causes direct relaxation of arteriolar smooth muscle, possibly secondary to a fall in intracellular Ca concentrations. The drug does not dilate epicardial coronary arteries or relax venous smooth muscle. Hydralazine-induced vasodilation is associated with powerful stimulation of the sympathetic nervous system, likely due to baroreceptor-mediated reflexes, which results in increased heart rate and contractility, increased plasma renin activity, and fluid retention all of these effects counteract the antihypertensive effect of hydralazine. Although most of the sympathetic activity is due to a baroreceptor-mediated reflex, hydralazine may stimulate NE release from sympathetic nerve terminals and augment myocardial contractility directly. Most of hydralazine s effects are confined to the cardiovascular system the decrease in blood pressure after administration is associated with a selective decrease in vascular resistance in the coronary, cerebral, and renal circulations, with a smaller effect in skin and muscle. Because of preferential dilation of arterioles, postural hypotension is not common, and hydralazine lowers blood pressure equally in the supine and upright positions. 

NPY produces a variety of central nervous system effects, including increased feeding (it is one of the most potent orexigenic molecules in the brain), hypotension, hypothermia, respiratory depression, and activation of the hypothalamic-pituitary-adrenal axis. Other effects include vasoconstriction of cerebral blood vessels, positive chronotropic and inotropic actions on the heart, and hypertension. The peptide is a potent renal vasoconstrictor and suppresses renin secretion, but can cause diuresis and natriuresis. Prejunctional neuronal actions include inhibition of transmitter release from sympathetic and parasympathetic nerves. Vascular actions include direct vasoconstriction, potentiation of the action of vasoconstrictors, and inhibition of the action of vasodilators. 

Other evidence which has been adduced to support the significance of neurogenic factors in renal hypertension is the observation that the arterial pressures of normal and renal hypertensive dogs and rabbits were reduced to essentially the same level after complete destruction of the central nervous system (18,19). However, interpretation of the results obtained with this drastic procedure is difficult. Other workers have observed a sharp fall in pressure when the spinal cord was destroyed below C5 (the level of the fifth cervical vertebra) in renal hypertensive dogs, but the pressures returned to hypertensive levels as the acute effects of the operation wore off (32). Other experiments involving elimination of the central connections of the sympathetics by cervical cord section in the region of C7... 

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