Mechanism underlying mannitol-induced relaxation in isolated monkey cerebral arteries.

The addition of mannitol (25, 50, and 100 mM) increased osmotic pressures of the bathing media from 293 to 317, 340 and 383 mosmol, respectively, and elicited a dose-related relaxation in monkey cerebral artery strips precontracted with K+ or prostaglandin F2 alpha. This relaxation was attenuated by ouabain, amiloride, catalase and oxyhemoglobin but was not influenced by superoxide dismutase and indomethacin. Combined treatment of the strips exposed to ouabain and amiloride with catalase produced an additional inhibition.

Comparison of hypoxia-induced contraction in human, monkey, and dog coronary arteries.

In monkey coronary artery strips contracted with prostaglandin (PG) F2 alpha or K+, exchange of entire N2 for O2 in the gas aerating the bathing media produced a contraction. Endothelium denudation did not alter the response. Aspirin, indomethacin, and ONO 3708, a PG receptor antagonist, markedly inhibited the hypoxia-induced contraction, whereas superoxide dismutase and OKY 046, a thromboxane (Tx) A2 synthesis inhibitor, were ineffective.

Mechanism of neurally induced monkey mesenteric artery relaxation and contraction.

Physiological importance in vasodilator innervation alleviating noradrenergic neurogenic vasoconstriction has not been clarified. Isolated monkey mesenteric artery strips denuded of the endothelium responded to nerve stimulation by electrical pulses or nicotine with a contraction, which was potentiated by Ng-nitro-L-arginine, a nitric oxide synthesis inhibitor, but not by the D-enantiomer. The potentiation was abolished by L-arginine.

Mechanism of relaxation induced by K+ and nicotine in dog duodenal longitudinal muscle.

Dog duodenal longitudinal muscle strips precontracted with bradykinin responded to K+ (10 mM) with a transient relaxation, which was abolished by tetrodotoxin and oxyhemoglobin, but not influenced by atropine, ouabain and apamin. The induced relaxation was suppressed by treatment with 10(-5) M NG-nitro-L-arginine (L-NNA) a nitric oxide synthesis inhibitor, but not by the D-enantiomer. The inhibitory effect was antagonized by L- but not D-arginine.

Suppression by NG-nitro-L-arginine of relaxations induced by non-adrenergic, non-cholinergic nerve stimulation in dog duodenal longitudinal muscle.

In dog duodenal longitudinal muscle strips, transmural electrical stimulation (10 Hz, 15 sec) elicited a transient contraction, which was abolished by tetrodotoxin and atropine but potentiated by treatment with NG-nitro-L-arginine (L-NA), a nitric oxide (NO) synthesis inhibitor. The potentiation was reversed by L-arginine but not by its D-enantiomer. Acetylcholine-induced contractions were not influenced by L-NA.

Reciprocal regulation by putatively nitroxidergic and adrenergic nerves of monkey and dog temporal arterial tone.

In monkey and dog superficial temporal artery strips denuded of the endothelium, transmural electrical stimulation and nicotine produced a contraction that was abolished by phentolamine and potentiated by NG-nitro-L-arginine (L-NNA), a nitric oxide (NO) synthesis inhibitor. The potentiation was reversed by L-arginine but not by its D-enantiomer. The arteries treated with phentolamine and contracted with prostaglandin F2 alpha responded to the electrical stimulation and nicotine with relaxations that were abolished by tetrodotoxin and hexamethonium, respectively, and were markedly inhibited by L-NNA but not by D-NNA, atropine, and timolol.

Distribution of somatostatin-immunoreactive cell bodies and fibers in the neocortex of Macaca fuscata.

The distribution of somatostatin-immunoreactive cell bodies and processes was studied in the cerebral cortex of the macaque monkey (Macaca fuscata), by applying an immunohistochemical technique with a monoclonal antibody raised against somatostatin tetradecapeptide. Many somatostatin-immunoreactive cell bodies and processes were observed in all regions of the cerebral cortex, i.e.

Role of nitric oxide in neurally induced cerebroarterial relaxation.

Transmural electrical stimulation and nicotine produced a relaxation of dog cerebral artery strips denuded of endothelium, which was abolished by tetrodotoxin and hexamethonium, respectively, and also suppressed by treatment with NG-nitro-L-arginine (L-NA), a nitric oxide (NO) synthesis inhibitor. The inhibition was reversed by L-arginine but not by the D-enantiomer. L-NA also suppressed the endothelium-dependent relaxation by substance P but not the response to NO and nitroglycerin.

Comparison of responses to angiotensin II of dog mesenteric arteries and veins.

Responses to angiotensin II (AII), arachidonic acid (AA) and prostaglandin (PG) I2 were compared in helical strips of dog mesenteric arteries and veins. Arterial strips contracted in response to AII, whereas venous strips responded with a transient, slight contraction followed by a moderate relaxation. The peptide-induced responses were abolished by treatment with saralasin, but were not influenced by ONO3708, an inhibitor of vasoconstrictor PG actions, or by endothelium denudation.

Responses to dopamine of isolated human and monkey veins compared with those of the arteries.

Isolated human gastroepiploic vein tributaries responded to dopamine only with contractions, whereas the gastroepiploic artery branches in the same region of the omentum responded with relaxations. Treatment with phentolamine converted the vein contraction to a relaxation, which was not influenced by propranolol but was abolished by droperidol. The relaxation was converted to a contraction by SCH23390 but unaffected by domperidone.

Age-related changes in responses to nerve stimulation and catecholamines in isolated monkey cerebral arteries.

Mechanical responses to transmural electrical stimulation, nicotine, norepinephrine, and isoproterenol were compared in cerebral artery strips obtained from Japanese monkeys of different ages (1 mo, 1 yr, 4-7 yr, and greater than 7 yr old). Transmural electrical stimulation produced a contraction in the baby and juvenile monkey arteries contracted with prostaglandin F2 alpha, whereas the older monkey arteries responded to the stimulation with a relaxation. The stimulation-induced contraction was abolished or reversed to a relaxation by phentolamine; the relaxation was not influenced by propranolol and atropine but was abolished by tetrodotoxin, as was the response of the mature monkey arteries.

Influence of methylene blue and oxyhemoglobin on mammalian vascular responses to sodium nitroprusside and nitroglycerin.

Vasodilatory responses to sodium nitroprusside were compared with those to nitroglycerin in helical strips of blood vessels isolated from dogs, humans, monkeys, rats and guinea-pigs. Sodium nitroprusside relaxed arterial and venous strips contracted with prostaglandin F2 alpha in a dose-related manner, as did nitroglycerin. Relaxant responses to sodium nitroprusside and nitroglycerin were significantly greater in dog coronary arteries than in the mesenteric arteries.

Different modulation by cyclooxygenase inhibitors of the response to angiotensin II in monkey arteries and veins.

In coronary, renal and femoral arteries and mesenteric veins isolated from Japanese monkeys, tachyphylaxis to angiotensin (ANG) II (10(-7) M)-induced contraction rapidly developed. Contractions caused by ANG II in coronary arteries were attenuated by treatment with indomethacin and aspirin and also by endothelium denudation. Indomethacin inhibited the response of the arteries with and without endothelium to a similar extent.

Motor activity correlates negatively with free-running period, while positively with serotonin contents in SCN in free-running rats.

Free-running period of blinded rats kept in a cage with a running wheel varied markedly, while it varied little in rats kept in a cage without a running wheel. The mean free-running period of the former group is significantly shorter than that of the latter. In the former, the free-running period correlated negatively with motor activity, indicating that activity affects the free-running period.

Comparison of endothelium-dependent responses of monkey cerebral and temporal arteries.

1. Endothelium-dependency of vasodilator responses was compared in helical strips of monkey cerebral and superficial temporal arteries contracted with prostaglandin F2 alpha. Acetylcholine produced an endothelium-dependent relaxation in the temporal arteries, but did not consistently alter the tone of cerebral arteries.

Infection without antibody response in mother-to-child transmission of HTLV-I in rabbits.

The presence or absence of the anti-human T-cell leukemia virus type (HTLV-I) antibody and the HTLV-I proviral genome was examined in the offspring of inbred rabbits, which were born to HTLV-I carrier does. The results showed that not all offspring born to the carriers were infected and that not all the infected offspring seroconverted at the age of 10 weeks, which is similar to observations made in human carriers. The anti-HTLV-I antibody was assayed by indirect immunofluorescence in 55 offspring at the age of 10 weeks, which were born to B/J or (B/J x Chbb:HM)F1 seropositive HTLV-I carrier does.

Prevention by nicardipine of dog basilar artery spasm caused by oxyhemoglobin in vivo and in vitro.

Intravenous infusions of nicardipine in a dose insufficient to lower blood pressure prevented the generation of the basilar artery spasm provoked by oxyhemoglobin (oxyHb) injected intracisternally in anesthetized dogs. The plasma concentration of nicardipine was comparable to that sufficient to suppress the oxyHb-induced contraction in isolated dog basilar arteries. Nicardipine appears to be similarly effective in antagonizing the vasoconstrictor action of oxyHb in vivo and in vitro.

Analysis of the potentiating action of N(G)-nitro-L-arginine on the contraction of the dog temporal artery elicited by transmural stimulation of noradrenergic nerves.

Dog temporal artery strips without endothelium responded to transmural electrical stimulation with a contraction which was potentiated by NG-nitro-L-arginine (L-NNA). The noradrenaline-induced contraction and the release of 3H-noradrenaline were not affected. The stimulation-induced contraction was reversed to a relaxation by phentolamine.

Constrictor action of oxyhemoglobin in monkey and dog basilar arteries in vivo and in vitro.

Angiographic studies on anesthetized dogs and Japanese monkeys showed that oxyhemoglobin (HbO2) injected into the cisterna magna produced a constriction of the basilar artery; the maximal constriction was attained 2-4 h later. Intracisternal injections of autologous blood, prostaglandin (PG) E2 and PGF2 alpha also constricted the artery to a similar extent, although the peak response was obtained much later (approximately 1 wk) with blood and was earlier (approximately 20 min) with PGs. The vasoconstrictor action of HbO2 was almost abolished by treatment for 5 h with aspirin in dogs and monkeys, whereas treatment of dogs with OKY 046, a thromboxane A2 synthesis inhibitor, did not significantly alter the action.

Phylogenetic study of serotonin-immunoreactive structures in the pancreas of various vertebrates.

The distribution pattern of serotonin (5HT) in the pancreas was studied immunohistochemically by using a 5HT monoclonal antibody in various vertebrates including the eel, bullfrog, South African clawed toad, turtle, chicken, mouse, rat, guinea-pig, cat, dog and human. In all species examined, except the bullfrog, 5HT-like immunoreactivity was observed in nerve fibers, in endocrine cells, or in both. Positive nerve fibers were found in the eel, turtle, mouse, rat and guinea-pig.

Acidic fibroblast growth factor-like immunoreactivity in brain of Alzheimer patients.

Localization of acidic fibroblast growth factor (aFGF)-like immunoreactivity was examined in postmortem human brain tissue of Alzheimer and age-matched control cases using a rabbit polyclonal antibody specific for aFGF. In control cases, a small number of glial cells were stained very weakly in white but not in gray matter. In Alzheimer cases, some astrocytes were strongly stained for aFGF in both gray and white matter.

Efficacy and safety of clentiazem in patients with essential hypertension: results of an early pilot test.

The purpose of this study was to evaluate the antihypertensive effect of a new calcium antagonist, clentiazem, on inpatients or outpatients with essential hypertension. After blood pressure was stable and greater than 160/95 mmHg with placebo for at least a 2-week observation period, oral clentiazem was administered once daily and dosage was increased stepwise from 10 to 40 mg over 10 weeks. Blood pressure significantly decreased by the second week of the study, and this hypotensive effect was maintained until the eighth week.

Suppression of the cerebral vasospastic actions of oxyhemoglobin by ascorbic acid.

Oxyhemoglobin (Oxy-Hb) produced a concentration-dependent contraction of monkey, dog, and bovine cerebral artery strips. Treatment of Oxy-Hb with ascorbic acid suppressed the ability of Oxy-Hb to contract the arteries, especially in the monkey arteries. The ability of intracisternally applied Oxy-Hb to constrict the basilar artery in anesthetized dogs was diminished when Oxy-Hb was treated previously with ascorbic acid (AsA-Hb).