| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1991: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1990: ¥1,100,000 (Direct Cost: ¥1,100,000)
|
|---|
| Research Abstract |
Arteries isolated from rats were suspended in physiological salt solution and beta-adrenoceptor (AR)-mediated vasorelaxation was investigated. It was found that beta-AR in femoral arteries and aortas were of beta, and beta_2 subtypes, respectively. Effects of norepinephrine (NE) on blood vessels were summation of alpha-AR-mediated vasoconstriction and beta-AR-mediated vasorelaxation. The contractile response of the femoral artery to NE was potentiated by propranolol and atenolol but not butoxamine. On the other hand, the contractile response of the aorta to NE was increased by butoxamine. Thus, it was found that vascular effects of NE, an adrenergic neurotransmitter, were modulated by activities of beta_1- and, beta_2-AR, in the femoral artery and aorta, respectively.
Rats were treated substaneously with some drugs for 7-10 days. Femoral arteries isolated from these rats were suspended in physiological salt solution. In vitro response to NE (mediated through beta_1-AR) were potentiated by subcutaneous propranolol and attenuated by subcutaneous isoproterenol. Thus, it was found that beta_1-AR-mediated effects were modulated by systemic administration of beta-AR agonists and antagonists
On femoral arteries of spontaneously hypertensive rats, it was found that vasoconstriction effects of NE were increased by decrease in beta_1-AR-mediated response.
In summary, it was suggested that systemic administration of drugs modulates beta-AR activity leading to changes in vascular responses mediated through beta-AR.
|
