Changes in α2-adrenoceptors on vascular smooth muscle and neural membranes following hypertension induced by renal ischemia1

Ronald E. Weishaar, R Clinton Webb, Charles B. Smith

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

 α2-Adrenoceptors were characterized on neural and vascular membranes from 2-kidney-l-clip renal hypertensive (RHT) and normotensive (NT) rats. Rats were sacrificed 6 weeks after induction of renal ischemia, and the specific binding of 3H-clonidine to smooth muscle membranes from tail arteries and neural membranes from various brain regions was examined. Additionally, isometric contractions of helically cut tail artery strips produced by various ct-adrenoceptor agonists were measured. Scatchard analysis indicated an increased number of high-affinity binding sites on the smooth muscle membranes from RHT rats (Bmax = 43.5 ± 1.4 fmol/mg protein) compared to that from the NT rats (25.4 ± 3.8 fmol/mg protein). An increased contractile sensitivity to clonidine was also observed in tail artery strips from RHT rats (EC50 for RHT = 3.04 X KH M; NT = 1.52 X 10-7M). In neural tissue, the number of a^-adrenoceptor-binding sites was significantly increased in the locus coeruleus from RHT rats, but not in the amygdala, hypothalamus, parietal cortex, hippocampus or lower brain stem. These results demonstrate that renal ischemia produces changes in both peripheral and neural (^-adrenoceptor density. The increase in smooth muscle ai-adrenoceptors might also provide a partial explanation for the supersensitivity to adrenergic agonists in this model of hypertension.

Original languageEnglish (US)
Pages (from-to)187-198
Number of pages12
JournalPharmacology
Volume43
Issue number4
DOIs
StatePublished - Jan 1 1991
Externally publishedYes

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Renal Hypertension
Vascular Smooth Muscle
Adrenergic Receptors
Kidney
Membranes
Smooth Muscle
Tail
Clonidine
Ischemia
Arteries
Binding Sites
Adrenergic Agonists
Parietal Lobe
Isometric Contraction
Locus Coeruleus
Renal Artery
Amygdala
Surgical Instruments
Hypothalamus
Brain Stem

Keywords

  • Supersensitivity
  • α2-Adrenoceptors Hypertension Vascular smooth muscle Brain regions

ASJC Scopus subject areas

  • Pharmacology

Cite this

Changes in α2-adrenoceptors on vascular smooth muscle and neural membranes following hypertension induced by renal ischemia1. / Weishaar, Ronald E.; Webb, R Clinton; Smith, Charles B.

In: Pharmacology, Vol. 43, No. 4, 01.01.1991, p. 187-198.

Research output: Contribution to journalArticle

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AB -  α2-Adrenoceptors were characterized on neural and vascular membranes from 2-kidney-l-clip renal hypertensive (RHT) and normotensive (NT) rats. Rats were sacrificed 6 weeks after induction of renal ischemia, and the specific binding of 3H-clonidine to smooth muscle membranes from tail arteries and neural membranes from various brain regions was examined. Additionally, isometric contractions of helically cut tail artery strips produced by various ct-adrenoceptor agonists were measured. Scatchard analysis indicated an increased number of high-affinity binding sites on the smooth muscle membranes from RHT rats (Bmax = 43.5 ± 1.4 fmol/mg protein) compared to that from the NT rats (25.4 ± 3.8 fmol/mg protein). An increased contractile sensitivity to clonidine was also observed in tail artery strips from RHT rats (EC50 for RHT = 3.04 X KH M; NT = 1.52 X 10-7M). In neural tissue, the number of a^-adrenoceptor-binding sites was significantly increased in the locus coeruleus from RHT rats, but not in the amygdala, hypothalamus, parietal cortex, hippocampus or lower brain stem. These results demonstrate that renal ischemia produces changes in both peripheral and neural (^-adrenoceptor density. The increase in smooth muscle ai-adrenoceptors might also provide a partial explanation for the supersensitivity to adrenergic agonists in this model of hypertension.

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