Β‐adrenoceptor Mediated Secretion of Active and Inactive Renin in Conscious Sheep

Abstract

1. Beta-adrenoceptor linked regulation of plasma active and inactive renin was investigated in sheep with indwelling artery, vein and bladder catheters. Concurrent changes in renal function were also monitored. 2. The beta-adrenoceptor agonist isoprenaline (bolus intravenous (i.v.) dose 0.5 mg/kg, 0.05 microgram/kg per min) increased plasma active renin concentration within 15 min and reached a plateau increase of 306%. Initially plasma inactive renin remained unchanged but after 105 min it decreased. 3. The non-selective beta-adrenoceptor antagonist propranolol (bolus i.v. dose 4 mg/kg, 40 micrograms/kg per min) did not significantly alter basal plasma active renin but selectively reduced inactive renin. The absence of any change in active renin may reflect the relatively low level of stress-induced sympathetic activation in these conscious animals compared to equivalent studies carried out on human subjects. 4. Using the same dose schedules, propranolol completely blocked the isoprenaline-induced increases in plasma active renin secretion even though it had no effect on the basal active renin levels. 5. The selective beta 1-adrenoceptor antagonist atenolol (bolus i.v. dose 5 mg/kg) decreased basal plasma active renin by 24% (+ 135 min) but reduced plasma inactive renin by 75% compared to control. 6. Therefore, both a beta-adrenoceptor agonist (isoprenaline) and two beta-adrenoceptor antagonists (propranolol and atenolol) decreased plasma inactive renin concentration in conscious sheep. 7. These results are discussed in relation to the accompanying changes in arterial blood pressure and aspects of renal function.

Adrenergic Drugs Alter Both the Fluid Kinetics and the Hemodynamic Responses to Volume Expansion in Sheep

“…The associated peripheral vasodilation acted to decrease the cardiac atrial pressures, but their relative increase during volume loading was still very strong. Isoprenaline increases renin secretion and therefore has an antidiuretic effect [11].…”

Effect of low sodium intake and β-blockade on renin synthesis and secretion in mice with unilateral ureteral ligation

“…10 Studies have demonstrated that b-adrenergic agonists increase renin release. [11][12][13][14] A moderate increase in the renal sympathetic nerve activity produced by graded common carotid occlusion also stimulates renin secretion. This increase was prevented by b-adrenoceptor blockade or surgical denervation of the kidney.…”