Prostaglandin B2 (PGB2) may be formed from PGA2in vivo. The following study compares the effects of equivalent concentrations of PGA2 and PGB2 on systemic pressure, heart rate, airway resistance, cutaneous vascular resistance, and responses to sympathetic nerve stimulation and to norepinephrine and tyramine in the acutely denervated canine hind paw perfused with autologous blood at constant flow. Intra-arterial (i.a.) PGB2 (1 and 10 μg/min) produced concentration-dependent vasoconstriction. Fifteen minutes after PGB2 administration the pressor responses of the paw to sympathetic nerve stimulation were enhanced, whereas the pressor responses to norepinephrine and tyramine were unchanged. In contrast, low concentrations of PGA2 produced systemic and transient cutaneous dilation whereas the higher concentration (10 μg/min i.a.) produced systemic dilation and constriction of the acutely denervated paw. The pressor responses of the perfused paw to sympathetic nerve stimulation were enhanced with the higher infusion rate of PGA2. However, the pressor responses to norepinephrine and tyramine were unchanged during PGA2. In addition, PGB2, but not PGA2, increased airway resistance. These results suggest that: (1) PGB2 and PGA2 have different effects on systemic pressure and airway resistance but have similar effects on the cutaneous vascular bed; (2) both PGB2 and PGA2 selectively enhance neurotransmitter release from the catecholamine pool susceptible to activation by the nerve action potential; and (3) PGB2 is more potent in its ability to enhance neurotransmitter release than PGA2. The vasoconstriction and facilitation of sympathetic neurotransmission by PGA2 may be related to formation of PGB2 within the paw.
Inhibitory effect of FRC-8653, a Ca2+ channel blocker, on pressor responses to electrical sympathetic nerve stimulation(ESNS) in pithed SHR.
