Journal of Clinical Investigation · 1967 · 316 citations · 33 references
MedicineEndocrinologyPhysiologyMineral MetabolismNeuroendocrinologyRenal PathophysiologyAdrenal HormonesAutonomic Nervous SystemAutonomic Nervous System ResponsesBlood Pressure RegulationOrthostatic HypotensionRenal PhysiologyAdrenocortical SecretionAldosterone RegulationPlasma Renin ActivitySodium DepletionSympathetic ActivationSympathetic Nervous System PhysiologySympathetic Nervous System RegulationSympathetic Nervous System Responses
Evidence indicates that the sympathetic nervous system modulates renal and adrenal hormone secretion during upright posture and sodium depletion. The study proposes that upright posture and sodium depletion reduce effective plasma volume, thereby increasing sympathetic activity. Sympathetic activation induces renal arteriolar constriction, elevating renin release and subsequently aldosterone production. Catecholamine infusion and sympathetic stimulation raise renin and aldosterone, and upright posture or sodium depletion elicit similar rises in healthy subjects, but a patient with autonomic insufficiency shows no such responses unless catecholamines are administered.
Several lines of evidence have been developed indicating that the sympathetic nervous system may play a role in mediating the renal and adrenocortical secretory responses to upright posture and sodium deprivation. Despite concurrent increases in arterial blood pressure, the plasma renin activity of normal subjects increased both in response to the infusion of catecholamines (norepinephrine: epinephrine, 10:1) and in response to stimulation of the sympathetic nervous system by cold. Aldosterone excretion was also increased by catecholamine infusion. In normal subjects the stimuli of upright posture and of sodium depletion both resulted in increases in urinary catecholamines, plasma renin activity, and urinary aldosterone. A patient with severe autonomic insufficiency did not experience normal elevations of urinary catecholamines, plasma renin activity, or urinary aldosterone in response to upright posture or sodium deprivation, despite a substantial fall in arterial blood pressure. When orthostatic hypotension was prevented by infusion of catecholamines, however, increases in plasma renin activity and in aldosterone excretion were observed. We suggest that both upright posture and sodium depletion lead to decreases in effective plasma volume and increases in sympathetic nervous system activity. This increase in sympathetic activity is then responsible for an increase in renal afferent arteriolar constriction, leading to an increase in renin secretion and, ultimately, an increase in aldosterone secretion.
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Hypotensive Agents and Pressor Substances
John H. Laragh · JAMA · 1960 · 526 citations
Medicine, Endocrinology, Physiology +17
NEW PROCEDURES FOR MEASUREMENT OF HUMAN PLASMA ANGIOTENSIN AND RENIN ACTIVITY LEVELS.
R. Boucher, R Veyrat, de Champlain J et al. · PubMed · 1964 · 402 citations · Full text
Medicine, Nephrology, Physiology +3
The substance causing renal hypertension
E Braun-Menendez, Juan Carlos Fasciolo, Luis F. Leloir et al. · The Journal of Physiology · 1940 · 362 citations