M1 receptors in blood pressure-controlled ischemic spontaneously hypertensive rats

Hiroshi Hirata, Masato Asanuma, Ken Ichi Tanaka, Yoichi Kondo, Norio Ogawa

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Background and Purpose: Hypertension is a primary aggravating factor in cerebral infarction. An acute rise in blood pressure (BP) at the time of a stroke may be harmful to the brain in a hypertensive subject because both cerebral vascular structure and function are altered by hypertension. Muscarinic M1 receptors are concerned with memory and learning. We aimed to evaluate the effect of controlling BP in hypertensive subjects at the time of stroke with a biochemical index of brain damage. Methods: We gave a single dose of either the antihypertensive α-blocker phentolamine (2 mg/kg IP) or the calcium antagonist nicardipine (2 mg/kg IP) at the start of bilateral carotid artery occlusion to spontaneously hypertensive rats undergoing 3 hours of transient ischemia; we measured the time course of mean BP (MBP) and changes in the M1 receptor and its mRNA in three brain regions 2 weeks after the transient ischemia. Results: Administration of phentolamine or nicardipine not only significantly suppressed the ischemia-induced rise of MBP, it actually decreased MBP during ischemia. In an ischemic control group, M1 receptor binding decreased in the frontal cortex and M1 receptor mRNA increased in the hippocampus 2 weeks after the ischemia. In contrast, both phentolamine- and nicardipine-treated ischemic rats showed no changes in either index compared with sham-operated controls. Conclusions: Controlling BP during an ischemic insult attenuates ischemia-induced damage of M1 receptors in the brain of spontaneously hypertensive rats. These results suggest that a rapid intensive increase of BP at the time of a stroke may exacerbate brain damage in hypertensive individuals.

Original languageEnglish
Pages (from-to)1268-1272
Number of pages5
JournalStroke
Volume26
Issue number7
Publication statusPublished - Jul 1995

Fingerprint

Inbred SHR Rats
Ischemia
Blood Pressure
Nicardipine
Phentolamine
Brain
Stroke
Muscarinic M1 Receptors
Hypertension
Messenger RNA
Cerebral Infarction
Frontal Lobe
Carotid Arteries
Antihypertensive Agents
Blood Vessels
Hippocampus
Learning
Calcium
Control Groups

Keywords

  • calcium channel blockers
  • cerebral ischemia
  • hypertension
  • rats

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Neuroscience(all)
  • Clinical Neurology
  • Advanced and Specialised Nursing

Cite this

Hirata, H., Asanuma, M., Tanaka, K. I., Kondo, Y., & Ogawa, N. (1995). M1 receptors in blood pressure-controlled ischemic spontaneously hypertensive rats. Stroke, 26(7), 1268-1272.

M1 receptors in blood pressure-controlled ischemic spontaneously hypertensive rats. / Hirata, Hiroshi; Asanuma, Masato; Tanaka, Ken Ichi; Kondo, Yoichi; Ogawa, Norio.

In: Stroke, Vol. 26, No. 7, 07.1995, p. 1268-1272.

Research output: Contribution to journalArticle

Hirata, H, Asanuma, M, Tanaka, KI, Kondo, Y & Ogawa, N 1995, 'M1 receptors in blood pressure-controlled ischemic spontaneously hypertensive rats', Stroke, vol. 26, no. 7, pp. 1268-1272.
Hirata H, Asanuma M, Tanaka KI, Kondo Y, Ogawa N. M1 receptors in blood pressure-controlled ischemic spontaneously hypertensive rats. Stroke. 1995 Jul;26(7):1268-1272.
Hirata, Hiroshi ; Asanuma, Masato ; Tanaka, Ken Ichi ; Kondo, Yoichi ; Ogawa, Norio. / M1 receptors in blood pressure-controlled ischemic spontaneously hypertensive rats. In: Stroke. 1995 ; Vol. 26, No. 7. pp. 1268-1272.
@article{9feda318cda44010ab5e2f8f0cdea67a,
title = "M1 receptors in blood pressure-controlled ischemic spontaneously hypertensive rats",
abstract = "Background and Purpose: Hypertension is a primary aggravating factor in cerebral infarction. An acute rise in blood pressure (BP) at the time of a stroke may be harmful to the brain in a hypertensive subject because both cerebral vascular structure and function are altered by hypertension. Muscarinic M1 receptors are concerned with memory and learning. We aimed to evaluate the effect of controlling BP in hypertensive subjects at the time of stroke with a biochemical index of brain damage. Methods: We gave a single dose of either the antihypertensive α-blocker phentolamine (2 mg/kg IP) or the calcium antagonist nicardipine (2 mg/kg IP) at the start of bilateral carotid artery occlusion to spontaneously hypertensive rats undergoing 3 hours of transient ischemia; we measured the time course of mean BP (MBP) and changes in the M1 receptor and its mRNA in three brain regions 2 weeks after the transient ischemia. Results: Administration of phentolamine or nicardipine not only significantly suppressed the ischemia-induced rise of MBP, it actually decreased MBP during ischemia. In an ischemic control group, M1 receptor binding decreased in the frontal cortex and M1 receptor mRNA increased in the hippocampus 2 weeks after the ischemia. In contrast, both phentolamine- and nicardipine-treated ischemic rats showed no changes in either index compared with sham-operated controls. Conclusions: Controlling BP during an ischemic insult attenuates ischemia-induced damage of M1 receptors in the brain of spontaneously hypertensive rats. These results suggest that a rapid intensive increase of BP at the time of a stroke may exacerbate brain damage in hypertensive individuals.",
keywords = "calcium channel blockers, cerebral ischemia, hypertension, rats",
author = "Hiroshi Hirata and Masato Asanuma and Tanaka, {Ken Ichi} and Yoichi Kondo and Norio Ogawa",
year = "1995",
month = "7",
language = "English",
volume = "26",
pages = "1268--1272",
journal = "Stroke",
issn = "0039-2499",
publisher = "Lippincott Williams and Wilkins",
number = "7",

}

TY - JOUR

T1 - M1 receptors in blood pressure-controlled ischemic spontaneously hypertensive rats

AU - Hirata, Hiroshi

AU - Asanuma, Masato

AU - Tanaka, Ken Ichi

AU - Kondo, Yoichi

AU - Ogawa, Norio

PY - 1995/7

Y1 - 1995/7

N2 - Background and Purpose: Hypertension is a primary aggravating factor in cerebral infarction. An acute rise in blood pressure (BP) at the time of a stroke may be harmful to the brain in a hypertensive subject because both cerebral vascular structure and function are altered by hypertension. Muscarinic M1 receptors are concerned with memory and learning. We aimed to evaluate the effect of controlling BP in hypertensive subjects at the time of stroke with a biochemical index of brain damage. Methods: We gave a single dose of either the antihypertensive α-blocker phentolamine (2 mg/kg IP) or the calcium antagonist nicardipine (2 mg/kg IP) at the start of bilateral carotid artery occlusion to spontaneously hypertensive rats undergoing 3 hours of transient ischemia; we measured the time course of mean BP (MBP) and changes in the M1 receptor and its mRNA in three brain regions 2 weeks after the transient ischemia. Results: Administration of phentolamine or nicardipine not only significantly suppressed the ischemia-induced rise of MBP, it actually decreased MBP during ischemia. In an ischemic control group, M1 receptor binding decreased in the frontal cortex and M1 receptor mRNA increased in the hippocampus 2 weeks after the ischemia. In contrast, both phentolamine- and nicardipine-treated ischemic rats showed no changes in either index compared with sham-operated controls. Conclusions: Controlling BP during an ischemic insult attenuates ischemia-induced damage of M1 receptors in the brain of spontaneously hypertensive rats. These results suggest that a rapid intensive increase of BP at the time of a stroke may exacerbate brain damage in hypertensive individuals.

AB - Background and Purpose: Hypertension is a primary aggravating factor in cerebral infarction. An acute rise in blood pressure (BP) at the time of a stroke may be harmful to the brain in a hypertensive subject because both cerebral vascular structure and function are altered by hypertension. Muscarinic M1 receptors are concerned with memory and learning. We aimed to evaluate the effect of controlling BP in hypertensive subjects at the time of stroke with a biochemical index of brain damage. Methods: We gave a single dose of either the antihypertensive α-blocker phentolamine (2 mg/kg IP) or the calcium antagonist nicardipine (2 mg/kg IP) at the start of bilateral carotid artery occlusion to spontaneously hypertensive rats undergoing 3 hours of transient ischemia; we measured the time course of mean BP (MBP) and changes in the M1 receptor and its mRNA in three brain regions 2 weeks after the transient ischemia. Results: Administration of phentolamine or nicardipine not only significantly suppressed the ischemia-induced rise of MBP, it actually decreased MBP during ischemia. In an ischemic control group, M1 receptor binding decreased in the frontal cortex and M1 receptor mRNA increased in the hippocampus 2 weeks after the ischemia. In contrast, both phentolamine- and nicardipine-treated ischemic rats showed no changes in either index compared with sham-operated controls. Conclusions: Controlling BP during an ischemic insult attenuates ischemia-induced damage of M1 receptors in the brain of spontaneously hypertensive rats. These results suggest that a rapid intensive increase of BP at the time of a stroke may exacerbate brain damage in hypertensive individuals.

KW - calcium channel blockers

KW - cerebral ischemia

KW - hypertension

KW - rats

UR - http://www.scopus.com/inward/record.url?scp=0028989244&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028989244&partnerID=8YFLogxK

M3 - Article

C2 - 7604424

AN - SCOPUS:0028989244

VL - 26

SP - 1268

EP - 1272

JO - Stroke

JF - Stroke

SN - 0039-2499

IS - 7

ER -