Segmental heterogeneity in relaxation response to nitric oxide (NO) was examined using NO donor sodium nitroprusside (SNP) in second- (medium) and fourth-generation (small) ovine isolated intralobar pulmonary arteries. In vessels precontracted with serotonin, NO donors SNP and S-nitroso-N-acetylpenicillamine (SNAP) were more potent in relaxing medium, in comparison to the small, arteries. Soluble guanylyl cyclase (sGC) inhibitor [1,2,4]oxadiazolo-[4,3-a]quinoxaline-1-one (ODQ 3 microM) caused a profound inhibition of SNP relaxation in small as compared with medium-sized arteries. However, both basal and SNP (10 microM)-stimulated intracellular cyclic guanosine monophosphate (cGMP) content was identical in these 2 arterial segments. The Na,K-ATPase inhibitor ouabain (1 microM) had a marked inhibitory effect on SNP-mediated relaxation in both segments. There was no segmental difference in SNP (10 microM)-stimulated plasma membrane Na,K-ATPase activity and ouabain-sensitive Rb-uptake. 4-AP (1 mM), a relatively selective inhibitor of Kv channels, decreased the potency of SNP relaxation by about 10-fold in the medium-sized vessels. On the other hand, 4-AP was without effect on the vasodilator potency of SNP in small vessels. Interestingly, in the presence of 4-AP, SNP was equipotent in dilating both medium (pD2 = 5.80 +/- 0.07; Emax = 84 +/- 1.6%, n = 7) and small (pD2 = 5.74 +/- 0.15; Emax = 83 +/- 2.5%, n = 7) pulmonary arteries. In conclusion, the results of the present study suggest that Kv channels determine the segmental heterogeneity of NO-mediated relaxation in ovine pulmonary artery.
Thyrotropin releasing hormone (TRH) immunoreactive peptides occur in high concentration within rat ventral prostate and human semen. To extend these observations to human reproductive organs, tissue fragments from human prostates undergoing benign hypertrophy were obtained by transurethral resection or open surgery. Human prostate, seminal vesicles, testes, and epididymis were also obtained from cadavers within 24 hours postmortem. After tissue extraction, the total TRH immunoreactivity (TRH IR) was measured by TRH radioimmunoassay. The total TRH IR in autopsy seminal vesicles was significantly greater (P < 0.01) than in all other autopsy reproductive tissues. The mean autopsy TRH IR of prostate was not significantly different from that measured in prostatic tissue obtained at surgery. High pressure liquid chromatography of extracts of autopsy seminal vesicles, prostate, and testis revealed multiple peaks of TRH IR. The two major peaks corresponded to the two TRH‐homologous peptides of human semen and one of the minor peaks cochromatographed with synthetic TRH. The distribution of TRH IR in human reproductive tissues appears to be very different from that in the rat, where ventral prostatic TRH IR levels exceed that of any other reproductive tissue by one to two orders of magnitude.
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