Renal vascular resistance, renin release, and tubular salt reabsorption are all increased when sympathetic nerves to the kidney are active.
The sympathetic nervous system alters the cardiac output, peripheral vascular resistance, and renal function, all of which play significant roles in controlling arterial pressure under various circumstances. The system has a role in the pathogenesis of chronic arterial hypertension and is capable of significant acute pressor effects. Because of its limitless capacity to restore altered arterial pressure to its original level by increasing or decreasing water and electrolyte excretion in response to elevated or decreased systemic arterial pressure, the renal volume/pressure control system is regarded as dominating physiological long-term arterial pressure regulation.
Renal vascular resistance, renin release, and tubular salt reabsorption are all increased when sympathetic nerves to the kidney are active. By reversing the pressure-natriuresis curve, these acts contribute to long-term increases in arterial pressure. Renal sensory receptors provide signals that are transmitted by renal afferent neurons to the efferent sympathetic nervous system, which has an impact on the control of arterial pressure. The current paper's goal is to examine recent research that shows how the sympathetic nervous system and the kidneys interact in the pathophysiology of both experimental and real-world arterial hypertension.
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