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At least 1,171 records · Page 65Linked to original sources
PubMedDate not supplied

Neutral endopeptidase inhibition increases the potency of ANP in isolated rat pulmonary resistance vessels and isolated blood perfused lungs.

We have investigated the effects of the neutral endopeptidase inhibitor, SCH 42354, on the vasoreactivity of atrial natriuretic peptide (ANP) in rat isolated pulmonary resistance vessels (PRV) and isolated perfused lungs (IPL). PRV (n = 37) were mounted onto the jaws of a myograph and precontracted with PGF2alpha (100 mu M). Concentration-responses to ANP (0.17 to 340 nM) were determined before and after the addition of SCH 42354 (10, 30 and 100 nM). Each concentration of SCH 42354 caused a significant increase in potency (- log EC50) of ANP in isolated PRV. Lungs from normoxic rats (n = 13) were isolated and perfused with whole blood. An increase in pulmonary artery pressure was achieved by ventilating with an hypoxic gas mixture and concentration-responses obtained by incremental additions of ANP (40 nM to 12 mu M), before and after the addition of SCH 42354 (100 nM). SCH 42354 significantly increased the potency (- log EC50) of ANP in the rat IPL. ANP is partly metabolized by NEP. That an inhibitor of NEP increased the potency of ANP in isolated pulmonary vessels, and in isolated perfused whole lungs, suggested that SCH 42354 may be having a local action within the pulmonary vasculature.

Animals↗
PubMed1981

Influence of damage of hypothalamo-hypophysial neurosecretory system and adrenalectomy on the blood-brain barrier alteration during intracranial hypertension.

Short-term intermittent cerebral compression following the lesion of NSO, NPV or ME alone or with adrenalectomy, caused disturbances in cerebrovascular system. It was characterized by congestion of blood vessels or vasoparalysis with the damage of BBB. These symptoms were much more pronounced in animals in which ME lesion was combined with adrenalectomy. It seems that the decreased level of vasopressor peptides (VSP, Ox) and catecholamines(A, NA) in the blood could be related to the increased activity of cholinergic system and other substances which are responsible for the dilatation of vessels. It is quite possible that the mutual relation of the above mentioned neuro-humoral factors determine the threshold for cardiovascular and cerebrovascular response to cerebral shock. The breakdown of this threshold could occur at the last stage of intracranial hypertension, being expressed by insufficient control of cardiovascular system with the fall of blood pressure and paralysis of cerebral blood vessels, BBB damage, that eventually might lead to brain death.

Adrenal Glands↗
PubMed1996

Membrane depolarization by activation of prostaglandin E receptor EP3 subtype of putative serotonergic neurons in the dorsal raphe nucleus of the rat.

A whole-cell current-clamp study using a thin slice preparation of the rat brain was carried out to elucidate the function of prostaglandin E (PGE) receptor EP3 subtype in the dorsal raphe nucleus (DR), where mRNA of this subtype is highly expressed. Bath application of PGE2 or M&B 28767, an EP3 agonist, depolarized the membrane of the large DR neurons in a concentration-dependent manner between 10(-9) and 10(-6) M. These neurons showed hyperpolarization of membrane potential to 10 or 50 microM serotonin. Neither an EP2 receptor agonist, butaprost, an EP2/EP4 receptor agonist, 11-deoxy-PGE1, nor an EP1 receptor agonist, 17-phenyl-PGE2, had any effect on large DR neurons between 10(-9) and 10(-6) M. The M&B 28767-induced depolarization was observed in a Ca(2+)-free, high Mg2+ (5 mM) solution containing 0.3 microM tetrodotoxin, and occurred equally well when intracellular Cl- was replaced by gluconate. These results suggest that direct agonist-activation of EP3 receptor depolarizes the membrane by a cationic conductance, leading to excitation of DR neurons, and indicate a physiological implication that EP3 receptor may modulate the serotonergic inhibition of neuronal activities.

Alprostadil↗
PubMed1990

Effects of conformational constraint in 2- and 8-cycloleucine analogues of oxytocin and [1-penicillamine] oxytocin examined by circular dichroism and bioassay.

The analogues of oxytocin and [1-penicillamine]oxytocin, containing a cycloleucine (Cle) residue in position 2 or 8, were investigated by means of circular dichroism measurements in different solvents, and the results examined in terms of their biological activities. A cycloleucine residue in position 2 substantially reduces the free conformational space of the hormone 20-membered ring moiety (including the disulfide group), and stabilizes a conformation which is close to one of the possible conformations of oxytocin and involves a beta-turn. In position 8, the Cle residue affects the conformation of the Tyr2 side chain, apparently forcing it away from the space above the 20-membered disulfide ring. However, it does not appear that the Cle residue has any significant effect on the overall backbone conformation of the hormone. The steric effect of the penicillamine residue in position 1 on the conformation of the disulfide group and Tyr2 side chain from previous investigations is further confirmed. The synthesis and biological potency of [1-penicillamine, 8-cycloleucine]oxytocin is described. This analogue exhibits a strong inhibitory effect on the uterotonic activity of oxytocin in vitro. It also inhibited the vasopressor response to vasopressin.

Animals↗