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Antihypertensive Effect of Propranolol in Conscious Spontaneously Hypertensive Rats: Central Hemodynamics, Plasma Volume, and Renal Function During β‐Blockade with Propranolol

In order to obtain a better insight into the hemodynamic changes during β-blockade, we measured central hemodynamics, plasma volume, and renal function during both acute and long-term β-blockade in conscious spontaneosly hypertensive rats (SHR). Acutely, both I and 5 mg/kg propranolol immediately decreased heart rate (HR) and cardiac output (CO). However, total peripheral resistance (TPR) rose sharply, thus preventing mean arterial pressure (MAP) from falling during the first hours after injection. After 4 h TPR had returned to control values and, because CO was still reduced, MAP was lowered. This decrease of MAP persisted for more than 20 h. During 5-day infusion of propranolol (5 mg/kg/day) CO fell on the 1st day and remained lowered during the 5-day period. MAP was lowered from the second day onward. Despite the reduced CO and MAP. plasma volume (PV) did not increase during the 5-day infusion. Acute injection of 5 mg/kg/day did, however, result in a decreased PV at 1 h postinjection. In this time span central venous pressure remained unchanged. Quantitation of water and sodium excretion revealed an immediate diuresis and natriuresis after acute administration of propranolol. This occurred despite a reduced glomerular nitration rate and effective renal plasma flow, as quantitated by indicator clearance methods. We conclude that propranolol reduced tubular sodium reabsorption, possibly through blockade of tubular β-receptors. This effect may be essential for the long-term antihypertensive efficacy of β-blockers because it prevents sodium and water retention in a state of reduced MAP and CO.