Analysis of vascular responses in rat hindquarters arterial resistance vessels and veins in situ
Sybertz, E.J.; Baum, T.; Williams, P.; Tedesco, R.P.; Sabin, C.
Journal of Pharmacology and Experimental Therapeutics 236(2): 374-379
1986
ISSN/ISBN: 0022-3565 PMID: 3003342 Document Number: 271547
The venous compartment plays a critical role in circulatory control. The present series of experiments was conducted to assess simultaneously effects of vasoactive drugs on arterial resistance and venous capacitance vessels of the rat hindquarters perfused with physiological salt solutions (SS). Retrograde infusion of SS into rat hindquarters via the vena cava resulted in an increase in hindquarters venous pressure (Pv). The range of mean volumes required to increase Pv to 20 and 30 mm Hg was 1.7 .+-. 0.1 to 2.9 .+-. 0.4 and 3.8 .+-. 0.3 to 6.9 .+-. 0.3 ml, respectively, in various groups of rats during a control period. Perfusion of the hindquarters with an SS containing 80 mM K+ reduced the volume required to increase Pv to 20 and 30 mm Hg to 47 .+-. 2 and 42 .+-. 2% of control, respectively, indicating venoconstriction. K+ (80 mM) SS also increased arterial perfusion pressure (Pa; measured from a sidearm off of the inflow catheter) to 141 .+-. 9 mm Hg, indicating arterial vasoconstriction. Arterial and venous responses to 80 mM K+ were attenuated markedly by perfusion with SS containing zero Ca and 2 mM ethylene glycol bis(.beta.-aminoethyl ether)-N,N'-tetraacetic acid, indicating dependence on extracellular Ca. Phentolamine (10-5 M) attenuated the arterial and venous response to 80 mM K+, indicating an alpha adrenergic contribution. Arterial responses to 80 mM K+ were attenuated markedly by the Ca entry blockers nifedipine (10-6 and 10-5 M) and verapamil (10-6 and 10-5 M). In contrast, venous responses were not affected by nifedipine and were reduced slightly only at the high concentration of verapamil. Nitroprusside (5 .times. 10-5 M) and nitroglycerin (10-4 M) attenuated arterial and venous responses to 80 mM K+. Hydralazine (10-4 M) did not affect either the arterial or venous responses. Perfusion of hindquarters with norepinephrine (NE) (7 .mu.M) also increased Pa (to 119 .+-. 8 mm Hg) and decreased venous capacitance to 51 .+-. 3 and 36 .+-. 2% of control at 20 and 30 mm Hg Pv, respectively. NE-induced vasoconstriction was attenuated by perfusion with zero Ca SS containing 2 mM ethylene glycol bis(.beta.-aminoethyl ether)-N,N'-tetraacetic acid. Nifedipine (10-7 to 10-5 M) and verapamil (10-6 and 10-5 M) attenuated markedly the increase in Pa to NE but did not affect the reduction of venous compliance. Nitroglycerin and nitroprusside inhibited arterial and venous responses to NE. Propranolol was without effect. The results suggest that vasoconstriction in the hindquarters resistance vessels is highly sensitive to extracellular Ca and Ca entry blockers. In contrast, venoconstriction is relatively insensitive to Ca entry blockers. Nitroglycerin and nitroprusside interfere effectively with both arterial and venous constriction. The data suggest that mechanisms of contraction and relaxation in hindquarters resistance and capacitance vessels differ.