TY - JOUR
T1 - Preserved cardiac β-adrenergic sensitivity in early renovascular hypertension
AU - Davidson, William R.
AU - Kawashima, Seinosuke
AU - Banerjee, Shailesh P.
AU - Liang, Chang Seng
PY - 1987/5
Y1 - 1987/5
N2 - To determine the mechanism of blunted sympathetic reflex responses in early renovascular hypertension, we measured inotropic and chronotropic responses of the heart to β-adrenergic stimulation in vivo and myocardial β-adrenergic receptor number and adenylate cyclase activity in 10 dogs during an early stage of one-kidney renal hypertension. Mean aortic pressure was higher hi the hypertensive dogs (152 ± 4 mm Hg) than in eight sham-operated dogs (122 ± 1 mm Hg; p < 0.001), but heart rate, cardiac output, and left atrial pressure did not differ between the two groups. Blood pressure reduction with a direct-acting vasodilator, pinacidil, resulted in marked increases in heart rate (+97 ± 12 beats/mm) and rate of change of left ventricular pressure (dP/dt; +1447 ± 367 mm Hg/sec) in normotensive dogs but only blunted heart rate (+54 ± 12 beats/min) and minimal left ventricular dP/dt (+376 ± 264 mm Hg/sec) responses in hypertensive dogs. In contrast, intravenously administered isoproterenol produced similar increases in heart rate and left ventricular dP/dt in the two groups. These two groups also did not differ in either left ventricular β-adrenergic receptor number and affinity or basal, isoproterenol-stimulated, and fluoride-stimulated adenylate cyclase activity. Thus, despite blunted reflex responses to blood pressure reduction, hypertensive dogs showed neither reduction in chronotropic and inotropic responses to direct β-adrenergic stimulation nor β-adrenergic desensitization of the myocardium, as assessed by β-adrenergic receptor number and adenylate cyclase activity. Blunted reflex responses in this model of early hypertension must be due to factors operating at some locus other than the β-adrenergic receptor-adenylate cyclase complex.
AB - To determine the mechanism of blunted sympathetic reflex responses in early renovascular hypertension, we measured inotropic and chronotropic responses of the heart to β-adrenergic stimulation in vivo and myocardial β-adrenergic receptor number and adenylate cyclase activity in 10 dogs during an early stage of one-kidney renal hypertension. Mean aortic pressure was higher hi the hypertensive dogs (152 ± 4 mm Hg) than in eight sham-operated dogs (122 ± 1 mm Hg; p < 0.001), but heart rate, cardiac output, and left atrial pressure did not differ between the two groups. Blood pressure reduction with a direct-acting vasodilator, pinacidil, resulted in marked increases in heart rate (+97 ± 12 beats/mm) and rate of change of left ventricular pressure (dP/dt; +1447 ± 367 mm Hg/sec) in normotensive dogs but only blunted heart rate (+54 ± 12 beats/min) and minimal left ventricular dP/dt (+376 ± 264 mm Hg/sec) responses in hypertensive dogs. In contrast, intravenously administered isoproterenol produced similar increases in heart rate and left ventricular dP/dt in the two groups. These two groups also did not differ in either left ventricular β-adrenergic receptor number and affinity or basal, isoproterenol-stimulated, and fluoride-stimulated adenylate cyclase activity. Thus, despite blunted reflex responses to blood pressure reduction, hypertensive dogs showed neither reduction in chronotropic and inotropic responses to direct β-adrenergic stimulation nor β-adrenergic desensitization of the myocardium, as assessed by β-adrenergic receptor number and adenylate cyclase activity. Blunted reflex responses in this model of early hypertension must be due to factors operating at some locus other than the β-adrenergic receptor-adenylate cyclase complex.
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U2 - 10.1161/01.HYP.9.5.467
DO - 10.1161/01.HYP.9.5.467
M3 - Article
C2 - 3032789
AN - SCOPUS:0023261072
VL - 9
SP - 467
EP - 472
JO - Hypertension
JF - Hypertension
SN - 0194-911X
IS - 5
ER -