Borkowski K R, Finch L
Clin Exp Hypertens (1978). 1978;1(2):279-91. doi: 10.3109/10641967809068609.
Bilateral injections of adrenaline (0.01-10.0 microgram) into the anterior hypothalamic (AH) region, in urethane-anaesthetised spontaneous hypertensive (SH) rats, elicited dose-dependent falls in blood pressure and heart rate. The bradycardia was immediately in onset while the hypotension was preceded by a short-lasting rise in blood pressure. Bilateral injections of adrenaline into the anterior preoptic area (POA) and areas surrounding the AH had little or no effect on blood pressure and heart rate, while injections into the posterior hypothalamus (PH) induced tachycardia and hypertension followed by a smaller fall in blood pressure. Pretreatment with dl-propranolol (25-100 microgram bilat. AH) appeared to potentiate the hypotension induced by adrenaline (1 microgram bilat. AH) in a dose-dependent manner, but did not affect the falls in heart rate. On the other hand, pretreatment with metoprolol (25-100 microgram bilat. AH) effected a dose-dependent antagonism of the adrenaline-induced hypotension and bradycardia. Pretreatment with 1-propranolol (25 microgram bilat. AH) also antagonised the adrenaline-induced cardiovascular depressor effects, while pretreatment with d-propranolol (25 microgram bilat. AH) abolished the initial hypertensive effect. Pretreatment with piperoxan (25-100 microgram bilat. AH) antagonised adrenaline (1 microgram bilat. AH) induced hypotension and bradycardia only at the highest dose used. The results give further support to the concept that hypothalamic adrenaline receptors may be involved in the central regulation of blood pressure and heart rate. Furthermore, while an involvement of hypothalamic alpha-adrenoceptors cannot be ruled out, it is suggested that hypothalamic beta-adrenoceptors may be involved in mediating the cardiovascular depressor effects of adrenaline injected into the AH.
在氨基甲酸乙酯麻醉的自发性高血压(SH)大鼠中,向前下丘脑(AH)区域双侧注射肾上腺素(0.01 - 10.0微克),可引起血压和心率呈剂量依赖性下降。心动过缓立即出现,而低血压之前有短暂的血压升高。向前视前区(POA)和AH周围区域双侧注射肾上腺素对血压和心率几乎没有影响,而向后下丘脑(PH)注射则诱发心动过速和高血压,随后血压有较小幅度下降。用dl - 普萘洛尔(双侧AH 25 - 100微克)预处理似乎以剂量依赖性方式增强了肾上腺素(双侧AH 1微克)诱导的低血压,但不影响心率下降。另一方面,用美托洛尔(双侧AH 25 - 100微克)预处理对肾上腺素诱导的低血压和心动过缓产生剂量依赖性拮抗作用。用1 - 普萘洛尔(双侧AH 25微克)预处理也拮抗了肾上腺素诱导的心血管降压作用,而用d - 普萘洛尔(双侧AH 25微克)预处理则消除了最初的升压作用。用哌罗克生(双侧AH 25 - 100微克)预处理仅在所用的最高剂量下拮抗肾上腺素(双侧AH 1微克)诱导的低血压和心动过缓。这些结果进一步支持了下丘脑肾上腺素受体可能参与血压和心率中枢调节的概念。此外,虽然不能排除下丘脑α - 肾上腺素受体的参与,但提示下丘脑β - 肾上腺素受体可能参与介导注入AH的肾上腺素的心血管降压作用。