Prostaglandin synthesis and renal vasoconstriction elicited by adrenergic stimuli are linked to activation of alpha-1 adrenergic receptors in the isolated rat kidney.

The authors have investigated the effect of norepinephrine (NE) and selective alpha-1, alpha-2 and beta adrenergic receptor agonists and antagonists on prostaglandin (PG) output and vascular tone to determine the type of adrenergic receptor involved in these biological actions of NE in the isolated rat kidney perfused at a constant flow rate with Tyrode's solution. Renal arterial administration of NE (0.32-3.2 nmol) and the selective alpha-1 adrenergic receptor agonists phenylephrine (3-29.5 nmol), cirazoline (0.5-4.6 nmol) and amidephrine (4.1-41 nmol) produced dose-related increases in PG output and perfusion pressure. Administration of the selective alpha-2 adrenergic receptor agonists B-HT 933 (2-20 nmol) and guanabenz (1.7-17 nmol) into the kidney produced only small increases in PG output and perfusion pressure, whereas another selective alpha-2 adrenergic receptor agonist xylazine (1-20 nmol) failed to increase perfusion pressure or PG output. Infusion of the beta adrenergic receptor agonist isoproterenol reduced perfusion pressure, but failed to increase the output of PGs. The selective alpha-1 adrenergic receptor antagonist prazosin (2.7 X 10(-6) M) inhibited PG output and renal vasoconstriction elicited by phenylephrine, cirazoline and amidephrine, but not that caused by B-HT 933 and guanabenz. In contrast, the selective alpha-2 adrenergic receptor antagonist rauwolscine (1.3 X 10(-6) M) inhibited the small rise in PG output and perfusion pressure elicited by B-HT 933 and guanabenz, but not that caused by NE, phenylephrine, cirazoline or amidephrine. The beta adrenergic receptor antagonist propranolol (3.86 X 10(-6) M) did not alter PG output or renal vasoconstriction produced by NE or alpha-1 and alpha-2 adrenergic receptor agonists.(ABSTRACT TRUNCATED AT 250 WORDS)