Baroreflexes prevent neurally induced sodium retention in angiotensin hypertension.
Recent studies indicate that renal sympathetic nerve activity is chronically suppressed during ANG II hypertension. To determine whether cardiopulmonary reflexes and/or arterial baroreflexes mediate this chronic renal sympathoinhibition, experiments were conducted in conscious dogs subjected to unilateral renal denervation and surgical division of the urinary bladder into hemibladders to allow separate 24-h urine collection from denervated (Den) and innervated (Inn) kidneys. Dogs were studied 1) intact, 2) after thoracic vagal stripping to eliminate afferents from cardiopulmonary and aortic receptors [cardiopulmonary denervation (CPD)], and 3) after subsequent denervation of the carotid sinuses to achieve CPD plus complete sinoaortic denervation (CPD + SAD). After control measurements, ANG II was infused for 5 days at a rate of 5 ng. kg(-1). min(-1). In the intact state, 24-h control values for mean arterial pressure (MAP) and the ratio for urinary sodium excretion from Den and Inn kidneys (Den/Inn) were 98 +/- 4 mmHg and 1.04 +/- 0.04, respectively. ANG II caused sodium retention and a sustained increase in MAP of 30-35 mmHg. Throughout ANG II infusion, there was a greater rate of sodium excretion from Inn vs. Den kidneys (day 5 Den/Inn sodium = 0.51 +/- 0.05), indicating chronic suppression of renal sympathetic nerve activity. CPD and CPD + SAD had little or no influence on baseline values for either MAP or the Den/Inn sodium, nor did they alter the severity of ANG II hypertension. However, CPD totally abolished the fall in the Den/Inn sodium in response to ANG II. Furthermore, after CPD + SAD, there was a lower, rather than a higher, rate of sodium excretion from Inn vs. Den kidneys during ANG II infusion (day 5 Den/Inn sodium = 2.02 +/- 0.14). These data suggest that cardiac and/or arterial baroreflexes chronically inhibit renal sympathetic nerve activity during ANG II hypertension and that in the absence of these reflexes, ANG II has sustained renal sympathoexcitatory effects.
Lohmeier
T E
TE
Departments of Physiology and Biophysics and Surgery (Cardiothoracic), University of Mississippi Medical Center, Jackson, Mississippi 39216, USA. tlohmeier@physiology.umsmed.edu
Lohmeier
J R
JR
Haque
A
A
Hildebrandt
D A
DA
D000804:Angiotensin II / Q000008:administration & dosage; D000818:Animals; D017704:Baroreflex / Q000502:physiology*; D002346:Carotid Sinus / Q000502:physiology / Q000503:physiopathology; D003714:Denervation; D004231:Diuresis; D004285:Dogs; D005260:Female; D006339:Heart Rate; D006439:Hemodynamics / Q000502:physiology*; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology*; D007668:Kidney / Q000294:innervation* / Q000503:physiopathology; D010656:Phenylephrine / Q000494:pharmacology; D011188:Potassium / Q000097:blood / Q000652:urine; D012083:Renin / Q000097:blood; D012849:Sinoatrial Node / Q000502:physiology; D012964:Sodium / Q000378:metabolism* / Q000652:urine; D013564:Sympathetic Nervous System / Q000503:physiopathology; D001743:Urinary Bladder / Q000502:physiology / Q000503:physiopathology*; D014630:Vagus Nerve / Q000502:physiology / Q000503:physiopathology
D000804:Angiotensin II; D010656:Phenylephrine; D012964:Sodium; D012083:Renin; D011188:Potassium