Decrease In Renal Nerve Activity Research Articles

Intravascular mechanoreceptor modulation of renal sympathetic nerve activity in the cat.

Experiments were performed in chloralose-anesthetized cats to characterize intravascular mechanoreceptro input to renal nerve activity in the intact and vagotomized sinoaortic-denervated states. High-pressure intravascular mechanoreceptors were stimulated by rises in arterial pressure caused by norepinephrine. Low-pressure intravascular mechanoreceptors were stimulated by progressive blood volume expansion (14-23%) at a rate of 4.4 or 17.6 ml/min. In addition, veratrine was used to stimulate directly both high- and low-pressure receptors. In the intact animal the administration of norepinephrine or blood volume expansion was associated with substantial decreases in renal nerve activity. Veratrine also caused a large dose-related decrease in renal nerve activity. However, in the vagotomized sinoaortic-denervated animal there was no change in renal nerve activity with norepinephrine, volume expansion, or veratrine administration. These experiments demonstrate that the major afferent pathways for renal sympathetic circulatory reflexes are confined to the carotid sinus and aortic and vagus nerves. No evidence was found for a significant contribution from sympathetic afferent nerves.

Characterization of high and low pressure baroreceptor influences on renal nerve activity in the primate Macaca fascicularis.

We characterized the influence of high pressure and low pressure intravascular receptors on renal nerve activity in the pentobarbital sodium-anesthetized nonhuman primate Macaca fascicularis. Epinephrine-induced increases in arterial pressure were used to stimulate high pressure receptors, and intravascular volume expansion was used to stimulate both high and low pressure receptors. In addition, the intravascular mechanoreceptors were stimulated directly by intravenous veratrine administration. All interventions produced large decreases in renal nerve activity in the intact state. Denervation of the carotid sinus or bilateral cervical vagal section dimished, whereas sinoaortic denervation with vagotomy completely abolished all responses of renal activity to these interventions. We conclude that the nonhuman primate possesses very sensitive renal nerve sympathetic reflexes that are modulated by intravascular mechanoreceptors whose afferents traverse the carotid sinus nerves and the vago-aortic trunks. The carotid sinus nerves and the vago-aortic trunks appear to be equally effective in inhibiting renal nerve activity in response to increases in arterial pressure. In addition, there are no afferent pathways mediating intravascular mechanoreceptor modulation of renal nerve activity outside the carotid sinus nerves and the vago-aortic trunks.

Acetylstrophanthidin-induced reflex inhibition of canine renal sympathetic nerve activity mediated by cardiac receptors with vagal afferents.

The present experiments were performed to determine whether digitalis-induced augmentation of cardiac receptor discharge could induce reflex reductions in renal sympathetic nerve activity. Intracoronary injection or epicardial application of acetylstrophanthidin (AS) in chloraloseanesthetized dogs caused large decreases in renal sympathetic nerve activity which were accompanied by modest decreases in heart rate and arterial pressure. Vagotomy prevented these reflex responses. Cholinergic blockade with atropine markedly attenuated the heart rate responses to AS but had little effect on the arterial pressure or renal nerve activity responses. Epicardial application of lidocaine blocked cardiac vagal afferents and the reflex responses to intracoronary AS. In sinoaortic denervated dogs, the relationships between doses of AS and mean arterial pressure, heart rate, and renal nerve activity responses were linear. Decreases in renal nerve activity were evoked by doses of AS which did not reflexly change heart rate or arterial pressure. These data show that AS can evoke reflex bradycardia, hypotension, and withdrawal of renal sympathetic nerve activity solely by augmenting the inhibitory influence of cardiac receptors with vagal afferents. This reflex effect may contribute to the changes in renal function and thus to the diuresis that occurs when heart failure is treated with digitalis.

Neural Control of Renal Tubular Sodium Reabsorption

Renal adrenergic nerves are in contact with the basement membranes of tubule cells and, when these nerves are stimulated or ablated, proximal tubular reabsorption of sodium is increased or decreased, respectively. Renal adrenergic nerve activity appears to be regulated by low-pressure cardiopulmonary receptors and high-pressure arterial baroreceptors in response to changes in blood volume. Thus, a decrease in blood volume or in effective circulating blood volume leads to an increase in renal nerve activity, release of norepinephrine, alpha-adrenergic stimulation and increased tubular reabsorption of sodium, whereas an increase in blood volume leads to a decrease in renal nerve activity, a decreased release of norepinephrine, an increased release of dopamine, possible beta-adrenergic stimulation and a decreased tubular reabsorption of sodium.