Blair M L, Gengo F M
Department of Physiology, University of Rochester School of Medicine, NY 14642, USA.
Can J Physiol Pharmacol. 1995 Aug;73(8):1198-202. doi: 10.1139/y95-171.
This study was designed to determine if tonic beta-adrenergic control of plasma renin activity (PRA) during dietary sodium restriction is due to stimulation of renal beta-adrenoceptors, extrarenal beta-adrenoceptors, or both. Experiments were performed in six conscious resting uninephrectomized dogs with chronically indwelling catheters in the aorta, vena cava, and remaining renal artery. The dogs were fed a low-sodium diet of approximately 7 mequiv. Na/day. PRA decreased by 28 +/- 4% of control (p < 0.01) when the beta-adrenoceptor antagonist propranolol was infused directly into the renal artery (ira) at a rate of 0.25 micrograms.kg-1.min-1 for 45 min, whereas iv propranolol infusion at the same rate had no effect on PRA. Propranolol infusion, 1 microgram.kg-1.min-1 iv, decreased PRA by 22 +/- 8% of control (p < 0.05) and produced significantly greater systemic beta-adrenoceptor blockade but a similar renal plasma propranolol concentration as with ira infusion, 0.25 micrograms.kg-1.min-1. Thus blockade of extrarenal beta-adrenoceptors produced no additional suppression of PRA beyond that which could be accounted for by blockade of renal beta-adrenoceptors. Therefore, suppression of PRA by propranolol is due solely to blockade of renal beta-adrenergic receptors in conscious sodium-deprived dogs.
本研究旨在确定饮食中钠限制期间，血浆肾素活性（PRA）的β-肾上腺素能紧张性控制是由于肾脏β-肾上腺素能受体、肾外β-肾上腺素能受体的刺激，还是两者皆有。实验在6只清醒、静息、单侧肾切除的犬中进行，这些犬的主动脉、腔静脉和剩余肾动脉中均长期留置导管。给这些犬喂食约7毫当量钠/天的低钠饮食。当以0.25微克·千克⁻¹·分钟⁻¹的速率将β-肾上腺素能受体拮抗剂普萘洛尔直接注入肾动脉（ira）持续45分钟时，PRA下降了对照值的28±4%（p<0.01），而以相同速率静脉输注普萘洛尔对PRA无影响。以1微克·千克⁻¹·分钟⁻¹的速率静脉输注普萘洛尔，使PRA下降了对照值的22±8%（p<0.05），并产生了明显更强的全身β-肾上腺素能受体阻滞，但肾血浆普萘洛尔浓度与以0.25微克·千克⁻¹·分钟⁻¹的速率经肾动脉输注时相似。因此，肾外β-肾上腺素能受体的阻滞除了可由肾脏β-肾上腺素能受体的阻滞所解释的之外，并未对PRA产生额外的抑制作用。所以，在清醒的缺钠犬中，普萘洛尔对PRA的抑制作用仅归因于肾脏β-肾上腺素能受体的阻滞。
