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To study the regulation of interactions between angiotensin II and its vascular smooth muscle receptor, we have investigated the effects of mono- and divalent cations and guanine nucleotides on 125I-angiotensin II binding to a particulate fraction of rat mesenteric artery. Relative to the control state (no added cations or nucleotides), radioligand binding was stimulated by divalent cations (Mn++ > Mg++ > Ca++) to a maximum of 350% of control (20 HIM Mn++). Binding was also increased to 125–150% of control by Na+ (50–150 ITIM), whereas binding was inhibited by other monovalent cations (Li+ » K+ = NH4+). The stimulatory effects of Na+ (50 miu) and Mn++ (<20 HIM) were additive, but only to the same maximal level attained in the presence of 20 ITIM Mn++(350% of control). Under control conditions, GTP and its nonhydrolyzable analogue, Gpp(NH)p, were equipotent in reducing 125I-angiotensin II binding (IC50 = 3 μM) whereas GDP, GMP, and ATP were much less potent. When endogenous divalent cations were chelated by EDTA (2 ITIM), binding was reduced by 25% and neither GTP nor Gpp(NH)p (1–500 μM) inhibited binding further, suggesting that divalent cations are required for guanine nucleotides to attenuate 12SI-angiotensin II binding. The effects of GTP and Gpp(NH)p varied as ambient cation concentrations changed. Scatchard analyses indicated a single class of binding sites with a control state equilibrium dissociation constant (Kd) of 5.5 ± 1.6 (SD) nM. The Mn++- or Na+-induced increase in binding was due to an increase in receptor affinity which was counteracted by Gpp(NH)p, binding capacity (Bmax) remaining constant. We conclude that cations and guanine nucleotides interact in one or more receptor-associated membrane sites, probably including the guanine nucleotide regulatory protein, to modulate the affinity of the vascular receptor for angiotensin II. This complex interplay of cations and guanine nucleotides to regulate binding may be involved in modulation of physiological smooth muscle responses to angiotensin II.

Sodium, divalent cations, and guanine nucleotides regulate the affinity of the rat mesenteric artery angiotensin II receptor.