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

C. L. Cooper, Kafait Malik

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Abstract

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. The effect of exogenous arachidonic acid (33 nmol) to enhance PG output was not altered by prazosin or rauwolscine; however, the cyclooxygenase inhibitor indomethacin abolished the output of PGs elicited by arachidonic acid or the adrenergic receptor agonists. These data indicate that PG synthesis and renal vasoconstriction elicited by NE are linked to activation of alpha-1 adrenergic receptors in the rat kidney.

Original languageEnglish (US)
Pages (from-to)24-31
Number of pages8
JournalJournal of Pharmacology and Experimental Therapeutics
Volume233
Issue number1
StatePublished - Jan 1 1985

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Adrenergic alpha-1 Receptors
Vasoconstriction
Adrenergic Agents
Prostaglandins
Kidney
Norepinephrine
Guanabenz
Adrenergic alpha-2 Receptor Agonists
Perfusion
Pressure
Phenylephrine
Adrenergic beta-Agonists
Adrenergic Antagonists
Yohimbine
Prazosin
Arachidonic Acid
Adrenergic alpha-1 Receptor Agonists
Adrenergic alpha-2 Receptor Antagonists
Adrenergic alpha-1 Receptor Antagonists
Adrenergic alpha-2 Receptors

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Pharmacology

Cite this

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title = "Prostaglandin synthesis and renal vasoconstriction elicited by adrenergic stimuli are linked to activation of alpha-1 adrenergic receptors in the isolated rat kidney",
abstract = "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. The effect of exogenous arachidonic acid (33 nmol) to enhance PG output was not altered by prazosin or rauwolscine; however, the cyclooxygenase inhibitor indomethacin abolished the output of PGs elicited by arachidonic acid or the adrenergic receptor agonists. These data indicate that PG synthesis and renal vasoconstriction elicited by NE are linked to activation of alpha-1 adrenergic receptors in the rat kidney.",
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N2 - 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. The effect of exogenous arachidonic acid (33 nmol) to enhance PG output was not altered by prazosin or rauwolscine; however, the cyclooxygenase inhibitor indomethacin abolished the output of PGs elicited by arachidonic acid or the adrenergic receptor agonists. These data indicate that PG synthesis and renal vasoconstriction elicited by NE are linked to activation of alpha-1 adrenergic receptors in the rat kidney.

AB - 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. The effect of exogenous arachidonic acid (33 nmol) to enhance PG output was not altered by prazosin or rauwolscine; however, the cyclooxygenase inhibitor indomethacin abolished the output of PGs elicited by arachidonic acid or the adrenergic receptor agonists. These data indicate that PG synthesis and renal vasoconstriction elicited by NE are linked to activation of alpha-1 adrenergic receptors in the rat kidney.

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