Pharmacological characterization of alpha1-adrenoceptor subtypes in the bovine tail artery.

Ioudina, M. V., Dyer, D. C. Pharmacological characterization of alpha1-adrenoceptor subtypes in the bovine tail artery. J. vet. Pharmacol. Therap. 25, 363-369. The purpose of this study was to identify the alpha1-adrenoreceptor subtypes present in the bovine tail artery which mediate contractions to adrenergic agonists. A61603, an alpha1A-selective agonist, was more potent compared with norepinephrine and phenylephrine. The pKA value of A61603 was 6.93 +/- 0.19 microM (n=6). Antagonists, BMY 7378, WB 4101 and 5-methylurapidil, caused a parallel shift to the right of the concentration-response curve to A61603 with pA2 values of 6.62, 9.27 and 8.86, respectively. Prazosin, BMY 7378 and WB 4101 inhibited phenylephrine induced contraction with pA2 values of 9.47, 7.17 and 9.73, respectively. The pA2 values obtained for 5-methylurapidil, WB 4101, BMY 7378 and prazosin against alpha1-adrenoceptor agonists were significantly correlated with pKi values (Zhu, Zhang & Han, 1997, Eur. J. Pharmacol.329, 55-61) for the cloned alpha1a-adrenoceptor but not with the cloned alpha1b- or alpha1d-adrenoceptor. BMY 7378, a selective alpha1D-adrenoceptor antagonist, was significantly more potent against the nonsubtype selective agonist phenylephrine than to A61603. Chloroethylclonidine (50 microM for 10 min) did not affect contractile responses to A61603, but caused a significant inhibition of contractile responses to phenylephrine. In conclusion, it appears that alpha1A- and alpha1D-adrenoceptors play a role in adrenergic mediated contraction in the bovine tail artery.

Effects of exercise training mode on the cardiovascular responses to lower body negative pressure in males.

BACKGROUND: Endurance-trained males may be more prone to orthostatic hypotension than untrained subjects and this is reflected in differences in their cardiovascular responses to lower body negative pressure (LBNP). It is uncertain if the type of endurance training used affects these responses. HYPOTHESIS: Endurance-trained runners will differ from endurance-trained swimmers in their cardiovascular responses to LBNP. METHODS: Male intercollegiate cross country runners (XC, n = 9), sprinters (SP, n = 7) and swimmers (SW, n = 12) underwent exposures to -10, -20 and -40 mm Hg LBNP. Forearm blood flow, heart rate (HR) and blood pressure were measured throughout. Maximal oxygen consumption (VO2max) was determined separately via combined arm-and-leg cycle ergometry. RESULTS: The XC were more fit than the SW and SP (VO2max = 64.5 +/- 3.5 vs. 51.7 +/- 1.9, 49.5 +/- 2.4 ml.kg-1.min-1; x +/- SEM; p < 0.05). Resting mean arterial pressure (MAP, 93 +/- 3 mm Hg) and forearm vascular resistance (FVR; 26.2 +/- 6.0 units) did not differ significantly between groups although HR was 17 +/- 3 b.min-1 higher (p < 0.05) in SW vs. SP and XC. Neither the pulse pressure, MAP, HR, nor FVR responses to the LBNP exposures differed significantly between the 3 groups. Compared to rest, pulse pressure was reduced (p < 0.05) 14% at -40 mm Hg. Similarly, HR was increased (p < 0.05) 10% at -40 mm Hg. FVR increased (p < 0.05) with each increase in LBNP becoming 91% greater at -40 mm Hg vs. rest. CONCLUSIONS: These data suggest that the cardiovascular responses to LBNP up to -40 mm Hg do not differ in chronically exercising males training with different modalities.