Cardiovascular and body fluid changes after aortic baroreceptor deafferentation.
These experiments were performed to determine the role of fluid volume contraction in the compensatory cardiovascular response to an abrupt neurogenically mediated increase in systemic arterial blood pressure. Acute neurogenic hypertension was produced by selective aortic baroreceptor deafferentation (ABD) in the rat. Salt and water balance, fluid compartment volumes, and arterial pressure were measured before and for 5 days after the induction of hypertension by ABD. In rats with ABD, arterial pressure was increased approximately 30 mmHg 1 day after deafferentation and declined 15-20 mmHg over the next 4 days. Plasma volume and extracellular fluid volume were decreased 5 days after ABD. Urine output did not increase after ABD, and the fluid volume contraction was instead the result of a significant decrease in water intake. Sham-operated rats did not exhibit significant changes in any of these parameters. Sodium balance decreased slightly in both sham-operated and ABD rats postsurgery. These results confirm that fluid volume contraction is a prominent compensatory response to an abrupt rise in arterial pressure, but suggest that this compensation is not necessarily mediated through alterations in renal salt and water excretion.
D000344:Afferent Pathways / Q000502:physiology; D000818:Animals; D001011:Aorta / Q000294:innervation; D001826:Body Fluids / Q000502:physiology*; D003714:Denervation; D004231:Diuresis; D006439:Hemodynamics; D006973:Hypertension / Q000503:physiopathology; D008297:Male; D011311:Pressoreceptors / Q000502:physiology*; D051381:Rats; D014882:Water-Electrolyte Balance