Nitric oxide regulation of monkey myometrial contractility.

1. We evaluated the effect of the nitric oxide (NO) donor CysNO (S-nitroso-L-cysteine) and endogenous NO upon spontaneous contractility in non-pregnant cynomolgus monkeys. We also assessed the role of intracellular guanosine 3',5'-cyclic monophosphate ([cyclic GMP]i) as a second messenger for NO in monkey uterine smooth muscle.

Functional and molecular expression of volume-regulated chloride channels in canine vascular smooth muscle cells.

1. We examined the possibility of functional and molecular expression of volume-regulated Cl- channels in vascular smooth muscle using the whole-cell patch-clamp technique and quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) on cells from canine pulmonary and renal arteries. 2.

Cyclic GMP-independent effects of nitric oxide on guinea-pig uterine contractility.

1. The role of nitric oxide (NO) in the regulation of uterine contractility has yet to be clearly defined. We evaluated the effect of NO (in the form of S-nitroso-cysteine, CysNO) upon uterine contractility and guanosine 3',5'-cyclic monophosphate (cyclic GMP) accumulation in pregnant and nonpregnant guinea-pig myometrium.

Adenosine-stimulated contraction in nonpregnant guinea pig myometrium does not involve cyclooxygenase.

Cyclooxygenase products are thought to mediate adenosine-stimulated contraction of nonpregnant myometrium. We have examined the effects of the cyclooxygenase inhibitors, indomethacin and meclofenamate, upon adenosine-stimulated contractions in isolated, endometrium-free strips of uterine smooth muscle from virgin guinea pigs. Indomethacin (30 microM) had no effect on adenosine-induced contractions; addition of meclofenamate at 30 microM, however, rapidly and reversibly blocked contractions in response to adenosine, yet had no effect upon acetylcholine-stimulated contractions.