Pressor actions of arginine vasopressin in pithed sprague-dawley, wistar-kyoto and spontaneously hypertensive rats before and after treatment with nifedipine or pertussis toxin

Reza Tabrizchi, Christopher Triggle

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

The pressor actions of arginine vasopressin (AVP) were examined in pithed Sprague-Dawley and Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). Prior to pithing, systolic blood pressure (SBP) and diastolic blood pressure (DBP) were recorded via an intra-arterial catheter from sodium pentobarbital anaesthetized rats. SBP and DBP recorded from SHR were significantly greater than those from Sprague-Dawley and WKY rats. However, after pithing, there were no significant differences between DBP among the various strains. Pertussis toxin pretreatment significantly reduced the prepithing SBP and DBP of the SHR but not Sprague—Dawley or WKY rats. Administration of nifedipine significantly reduced DBP of pithed rats. The dose—diastolic pressure response curves obtained from infusion of AVP in Sprague-Dawley and WKY rats were not significantly different from one another, but the maximal vasopressor responses to AVP in pithed SHR were enhanced. Administration of nifedipine to Sprague-Dawley and WKY rats did not affect the dose-response curve to AVP, but nifedipine administration in SHR led to a significant inhibition of the pressor responses to AVP. Furthermore, pertussis toxin pretreament of rats significantly reduced a component of the AVP pressor effect in SHR but not Sprague-Dawley or WKY rats. We speculate that, in SHR, vasopressin receptors are coupled to a pertussis toxin-sensitive G protein that, in turn, may couple to a dihydropyridine-sensitive calcium channel and also to a pertussis-insensitive G protein that is probably coupled to the phospholipase C/intracellular calcium release process. A component of the elevated blood pressure in SHR is also regulated by a pertussis toxin-sensitive process. However, this toxin does not have a significant effect on the blood pressure of Sprague-Dawley or WKY rats, suggesting that there is a pertussis toxin-sensitive receptor and/or channel which is differentially expresse.

Original languageEnglish
Pages (from-to)813-818
Number of pages6
JournalJournal of Hypertension
Volume9
Issue number9
Publication statusPublished - 1991
Externally publishedYes

Fingerprint

Arginine Vasopressin
Pertussis Toxin
Inbred SHR Rats
Nifedipine
Blood Pressure
Inbred WKY Rats
GTP-Binding Proteins
Vasopressin Receptors
Whooping Cough
Type C Phospholipases
Pentobarbital
Calcium Channels

Keywords

  • Calcium antagonist
  • Pertussis toxin
  • Spontaneously hypertensive rats
  • Vasopressin

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Internal Medicine
  • Endocrinology

Cite this

@article{672dd3964ebb430b89c6dc3914defd6e,
title = "Pressor actions of arginine vasopressin in pithed sprague-dawley, wistar-kyoto and spontaneously hypertensive rats before and after treatment with nifedipine or pertussis toxin",
abstract = "The pressor actions of arginine vasopressin (AVP) were examined in pithed Sprague-Dawley and Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). Prior to pithing, systolic blood pressure (SBP) and diastolic blood pressure (DBP) were recorded via an intra-arterial catheter from sodium pentobarbital anaesthetized rats. SBP and DBP recorded from SHR were significantly greater than those from Sprague-Dawley and WKY rats. However, after pithing, there were no significant differences between DBP among the various strains. Pertussis toxin pretreatment significantly reduced the prepithing SBP and DBP of the SHR but not Sprague—Dawley or WKY rats. Administration of nifedipine significantly reduced DBP of pithed rats. The dose—diastolic pressure response curves obtained from infusion of AVP in Sprague-Dawley and WKY rats were not significantly different from one another, but the maximal vasopressor responses to AVP in pithed SHR were enhanced. Administration of nifedipine to Sprague-Dawley and WKY rats did not affect the dose-response curve to AVP, but nifedipine administration in SHR led to a significant inhibition of the pressor responses to AVP. Furthermore, pertussis toxin pretreament of rats significantly reduced a component of the AVP pressor effect in SHR but not Sprague-Dawley or WKY rats. We speculate that, in SHR, vasopressin receptors are coupled to a pertussis toxin-sensitive G protein that, in turn, may couple to a dihydropyridine-sensitive calcium channel and also to a pertussis-insensitive G protein that is probably coupled to the phospholipase C/intracellular calcium release process. A component of the elevated blood pressure in SHR is also regulated by a pertussis toxin-sensitive process. However, this toxin does not have a significant effect on the blood pressure of Sprague-Dawley or WKY rats, suggesting that there is a pertussis toxin-sensitive receptor and/or channel which is differentially expresse.",
keywords = "Calcium antagonist, Pertussis toxin, Spontaneously hypertensive rats, Vasopressin",
author = "Reza Tabrizchi and Christopher Triggle",
year = "1991",
language = "English",
volume = "9",
pages = "813--818",
journal = "Journal of Hypertension",
issn = "0263-6352",
publisher = "Lippincott Williams and Wilkins",
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T1 - Pressor actions of arginine vasopressin in pithed sprague-dawley, wistar-kyoto and spontaneously hypertensive rats before and after treatment with nifedipine or pertussis toxin

AU - Tabrizchi, Reza

AU - Triggle, Christopher

PY - 1991

Y1 - 1991

N2 - The pressor actions of arginine vasopressin (AVP) were examined in pithed Sprague-Dawley and Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). Prior to pithing, systolic blood pressure (SBP) and diastolic blood pressure (DBP) were recorded via an intra-arterial catheter from sodium pentobarbital anaesthetized rats. SBP and DBP recorded from SHR were significantly greater than those from Sprague-Dawley and WKY rats. However, after pithing, there were no significant differences between DBP among the various strains. Pertussis toxin pretreatment significantly reduced the prepithing SBP and DBP of the SHR but not Sprague—Dawley or WKY rats. Administration of nifedipine significantly reduced DBP of pithed rats. The dose—diastolic pressure response curves obtained from infusion of AVP in Sprague-Dawley and WKY rats were not significantly different from one another, but the maximal vasopressor responses to AVP in pithed SHR were enhanced. Administration of nifedipine to Sprague-Dawley and WKY rats did not affect the dose-response curve to AVP, but nifedipine administration in SHR led to a significant inhibition of the pressor responses to AVP. Furthermore, pertussis toxin pretreament of rats significantly reduced a component of the AVP pressor effect in SHR but not Sprague-Dawley or WKY rats. We speculate that, in SHR, vasopressin receptors are coupled to a pertussis toxin-sensitive G protein that, in turn, may couple to a dihydropyridine-sensitive calcium channel and also to a pertussis-insensitive G protein that is probably coupled to the phospholipase C/intracellular calcium release process. A component of the elevated blood pressure in SHR is also regulated by a pertussis toxin-sensitive process. However, this toxin does not have a significant effect on the blood pressure of Sprague-Dawley or WKY rats, suggesting that there is a pertussis toxin-sensitive receptor and/or channel which is differentially expresse.

AB - The pressor actions of arginine vasopressin (AVP) were examined in pithed Sprague-Dawley and Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). Prior to pithing, systolic blood pressure (SBP) and diastolic blood pressure (DBP) were recorded via an intra-arterial catheter from sodium pentobarbital anaesthetized rats. SBP and DBP recorded from SHR were significantly greater than those from Sprague-Dawley and WKY rats. However, after pithing, there were no significant differences between DBP among the various strains. Pertussis toxin pretreatment significantly reduced the prepithing SBP and DBP of the SHR but not Sprague—Dawley or WKY rats. Administration of nifedipine significantly reduced DBP of pithed rats. The dose—diastolic pressure response curves obtained from infusion of AVP in Sprague-Dawley and WKY rats were not significantly different from one another, but the maximal vasopressor responses to AVP in pithed SHR were enhanced. Administration of nifedipine to Sprague-Dawley and WKY rats did not affect the dose-response curve to AVP, but nifedipine administration in SHR led to a significant inhibition of the pressor responses to AVP. Furthermore, pertussis toxin pretreament of rats significantly reduced a component of the AVP pressor effect in SHR but not Sprague-Dawley or WKY rats. We speculate that, in SHR, vasopressin receptors are coupled to a pertussis toxin-sensitive G protein that, in turn, may couple to a dihydropyridine-sensitive calcium channel and also to a pertussis-insensitive G protein that is probably coupled to the phospholipase C/intracellular calcium release process. A component of the elevated blood pressure in SHR is also regulated by a pertussis toxin-sensitive process. However, this toxin does not have a significant effect on the blood pressure of Sprague-Dawley or WKY rats, suggesting that there is a pertussis toxin-sensitive receptor and/or channel which is differentially expresse.

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