Key result
Renovascular hypertension significantly diminished the inotropic responsiveness to isoproterenol (11.77 vs 27.39 g X mm-2 X s-1; P<0.05) without altering beta-receptors.
Why the study?
Does renovascular hypertension impair inotropic responsiveness to beta-adrenergic stimulation in male Wistar rats?
Does renovascular hypertension impair inotropic responsiveness to beta-adrenergic stimulation in male Wistar rats?
Absolute Event Rate: 11.77% vs 27.39%
p-value: p=<0.05
Early-stage renal hypertension impairs the inotropic response to isoproterenol without altering beta-receptor number or affinity, suggesting a postreceptor defect.
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May indicate postreceptor beta-adrenergic defect in experimental hypertension; hypothesis-generating for human renovascular disease.
Gende et al. (1985) studied Renovascular hypertension. Renovascular hypertension (2-kidney, 1-clip Goldblatt) vs. Age-matched normotensive controls was evaluated on Maximum increase in the maximal rate of rise of tension produced by isoproterenol (p=<0.05). Renovascular hypertension significantly diminished the inotropic responsiveness to isoproterenol (11.77 vs 27.39 g X mm-2 X s-1; P<0.05) without altering beta-receptors.
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