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DEMONSTRATION OF PROXIMAL TUBULAR α‐ADRENOCEPTORS IN VIVO
Author(s) -
Woodcock Elizabeth A.,
McLeod Jennifer K.,
Johnston Colin I.
Publication year - 1984
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1984.tb00287.x
Subject(s) - endocrinology , medicine , parathyroid hormone , chemistry , phentolamine , convoluted tubule , stimulation , agonist , clonidine , cyclase , receptor , kidney , biology , calcium
SUMMARY 1. Receptors for parathyroid hormone (PTH) in the renal tubule are coupled to adenylate cyclase stimulation. PTH causes a rise in urinary cAMP by leakage from cells of the proximal convoluted tubule. 2. The effects of α‐adrenergic agonists and antagonists on the urinary cAMP response to PTH were investigated in anaesthetized rats in vivo . Injection of PTH (15 u/kg i.v.) produced an increase in urinary cAMP from 1.7 (s.e.m. = 0.3, n = 6) to 7.47 (s.e.m. =0.7, n =6) nmol cAMP/μmol creatinine in 30 min urine samples. Infusion of the α 2 ‐adrenoceptor agonist clonidine at 1 μg/kg per min caused a decrease in the cAMP response to PTH to 3.6 (s.e.m. =0.5, n = 12) nmol cAMP/μmol creatinine. Infusion of the α 2 ‐selective catecholamine α‐methylnoradrenaline (1 μg/kg per min) caused a similar reduction in urinary cAMP response to that observed with clonidine. 3. The α‐adrenoceptor antagonist phentolamine (100 μg/kg per min) enhanced the cAMP response to PTH and reversed the decreased response caused by clonidine. 4. These results demonstrate the presence of α‐receptors in the rat proximal convoluted tubule which oppose the actions of PTH in vivo .