AJP - Heart and Circulatory Physiology, Vol 251, Issue 5 908-H914, Copyright © 1986 by American Physiological Society
Hemodynamic changes during onset of high-sodium one-kidney figure-8 renal hypertension
C. Hinojosa and J. R. Haywood
The hemodynamic changes associated with the onset of one-kidney, figure-8,
renal-wrap hypertension were monitored in rats fed a high-sodium diet. In
addition, the hemodynamic contributions of the sympathetic nervous system
(SNS) and arginine vasopressin (AVP) were assessed during the 1st week of
hypertension. Renal wrapping caused mean arterial pressure (MAP) to
increase significantly from 108 +/- 4 to 140 +/- 4 mmHg on day 5 after
renal surgery. The hypertension was associated with a significant
bradycardia and no significant change in cardiac output (CO), as measured
with an electromagnetic flow probe. Total peripheral resistance (TPR) was
significantly elevated to 140% above control value on day 5 after renal
surgery. Ganglionic blockade caused similar decreases in MAP and TPR in
normotensive and hypertensive animals. Sympathetic blockade after
pretreatment with a specific vascular antagonist of AVP,
[1-beta-mercapto-beta, beta-cyclopentamethylene propionic acid),
2-(O-methyl)tyrosine]Arg8-vasopressin ([d(CH2)5Tyr(Me)]AVP), caused a
greater depressor response in the renal-wrapped animals as compared with
the effect of ganglionic blockade alone in these animals. The effect of
[d(CH2)5Tyr(Me)]AVP alone on the hemodynamics was not different between the
two groups of rats. After ganglionic blockade pretreatment,
[d(CH2)5Tyr(Me)]AVP caused a significant decrease in MAP and TPR in the
renal-wrapped animals. In addition, the difference in MAP and TPR between
the two groups of rats was eliminated after combined blockade of AVP and
the SNS. The results of this study indicated that the onset of hypertension
was a result of an activation of neurohumoral mechanisms to increase
TPR.(ABSTRACT TRUNCATED AT 250 WORDS)
