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Biomedical subjects

H Jin

Publications and source records attributed to H Jin.

At least 271 records · Page 15Linked to original sources
PubMed1988

Exaggerated depressor response to 6-iodoamiloride in NaCl-sensitive spontaneously hypertensive rats.

The current study tested the hypothesis that NaCl-sensitive hypertension may result from increased membrane sodium channel activity. The effect of 6-iodoamiloride, and analog of the sodium channel blocker amiloride, on mean arterial pressure (MAP) was examined in conscious, freely moving NaCl-sensitive spontaneously hypertensive rats (SHR-S) fed high (8%) or normal (1%) NaCl diets. SHR-S and age-matched NaCl-resistant SHR (SHR-R) and normotensive Wistar-Kyoto (WKY) control rats were studied at 9 weeks of age after 2 weeks on either high (8%) NaCl or control (1%) NaCl diets. 6-iodoamiloride was infused intravenously in doses of 0.38 or 0.76 mg/100 g body weight, and MAP and heart rate (HR) were monitored from a femoral arterial cannula for 2 hours. The 8% NaCl diet caused a significant elevation in MAP in SHR-S but not in SHR-R or WKY. Administration of 6-iodoamiloride (both doses) produced a significant, sustained decrease in MAP in both SHR-S and SHR-R. Maximal depressor responses to high dose 6-iodoamiloride were significantly enhanced in SHR-S fed 8% NaCl (31.2 +/- 3.7 mm Hg) compared to SHR-S fed 1% NaCl (14.8 +/- 2.4 mm Hg) or SHR-R fed either 8% or 1% NaCl diets (15.6 +/- 4.2 and 10.2 +/- 3.0 mm Hg, respectively). In contrast, feeding an 8% NaCl diet had no significant effect on the depressor responses to 6-iodoamiloride in either SHR-R or WKY rats. In WKY, these doses of 6-iodoamiloride had no significant effect on MAP in either diet group. 6-iodoamiloride had no significant effect on heart rate in any group. These results support the hypothesis that the exacerbation of hypertension in SHR-S fed a high NaCl diet may result from increased membrane sodium channel activity.

Amiloride↗
PubMed1988

High NaCl diet reduces hypothalamic norepinephrine turnover in hypertensive rats.

The current study tested the hypothesis that high NaCl diets elevate blood pressure in NaCl-sensitive spontaneously hypertensive rats (SHR-S) by reducing noradrenergic input to depressor neurons in the anterior hypothalamus. SHR-S were studied at 7 weeks of age, and age-matched salt resistant SHR (SHR-R) and normotensive Wistar-Kyoto rats (WKY) were controls. Rats were fed either high (8%) NaCl or control (1% NaCl) diets for 2 weeks, following which norepinephrine turnover in hypothalamus (anterior, posterior, and ventral regions), brainstem (pons and medulla), and thoracic spinal cord was assessed using the dopamine beta-hydroxylase inhibitor 1-cyclohexyl-2-mercapto-imidazole (CHMI). Regional brain catecholamines were measured by high performance liquid chromatography with electrochemical detection following intraperitoneal injection of CHMI or vehicle. Disappearance of norepinephrine following CHMI was used as an index of noradrenergic neuronal activity. The 8% NaCl diet caused a significant elevation in blood pressure in SHR-S but not in SHR-R or WKY. Endogenous norepinephrine levels and turnover were lower in the anterior hypothalamus of SHR-S fed 8% NaCl than in those fed 1% NaCl but were not significantly different in other groups. Endogenous norepinephrine levels and turnover were greater in pons of 8% NaCl--fed SHR-S than in those fed 1% NaCl but were not significantly different in other groups. These observations support the hypothesis that reduced noradrenergic input to depressor neurons in the anterior hypothalamus and increased noradrenergic input to neurons in the pons are related to NaCl sensitivity in the SHR-S.

Animals↗
PubMed1987

Hypoxia-induced inhibition of converting enzyme activity: role in vascular regulation.

Systemic and pulmonary vascular reactivity to graded doses of angiotensin I (ANG I), angiotensin II (ANG II), and, as a control, phenylephrine were examined in 14- or 28-day hypoxia-exposed and air control rats. Hypoxic rats exhibited pulmonary hypertension that was reversible on return to room air, but systemic arterial pressure was not altered by hypoxia. Systemic pressor responses to ANG I and ANG II were significantly less in the hypoxic rats than in the control rats at 14 and 28 days but returned to control levels in hypoxic animals that were then returned to room air, demonstrating reversibility of the hypoxia-induced changes in vascular reactivity. Pulmonary pressor responses to ANG I were significantly less at 14 days, whereas responses to ANG II were significantly greater at 28 days, in hypoxic rats than in controls. There were no significant differences in systemic and pulmonary pressor responses to phenylephrine between the hypoxic and air control animals. The altered systemic and pulmonary pressor responsiveness to ANG I and ANG II in hypoxic rats is probably related to mechanisms specific to the renin-angiotensin system, such as inhibition of intrapulmonary angiotensin-converting enzyme activity and down regulation of ANG II receptors in the systemic circulation. Further study is needed to elucidate these mechanisms.

Angiotensin I↗
PubMed1987

Spontaneously hypertensive rats exhibit reduced hypothalamic noradrenergic input after NaCl loading.

Spontaneously hypertensive rats (SHR) of the Okamoto strain exhibit a significant exacerbation in severity of hypertension when fed diets high in NaCl. To examine the hypothesis that abnormalities in the monoaminergic innervation of the hypothalamus and brainstem contribute to the NaCl-induced exacerbation of hypertension, the monoamine and monoamine metabolite contents of specific hypothalamic and brainstem regions thought to be involved in the pathogenesis of hypertension were determined in SHR fed a diet containing 8% or 1% NaCl for either 2 or 6 weeks beginning at age 8 weeks. SHR maintained on the 8% NaCl diet for 2 weeks displayed significant decreases in norepinephrine in both the anterior and posterior hypothalamic regions but not in other brainstem or hypothalamic regions, as compared with animals consuming 1% NaCl. In addition, stores of the principal terminal norepinephrine metabolite 3-methoxy-4-hydroxyphenylglycol were reduced in the anterior hypothalamic region of SHR fed an 8% NaCl diet for 2 weeks. After 6 weeks on the diets, SHR fed 8% NaCl showed small but statistically nonsignificant reductions in norepinephrine stores of the anterior hypothalamic region as compared with SHR fed a basal diet, while WKY fed 8% NaCl had significantly elevated norepinephrine stores in the anterior hypothalamic region as compared with WKY fed a basal diet. There was a significant group X diet interaction (p less than 0.05). After 6 weeks on the 8% NaCl diet, SHR (but not WKY) displayed a significant reduction in norepinephrine content of the posterior hypothalamic region. No NaCl-induced differences in norepinephrine stores were found in the pons or medulla of either strain.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMedDate not supplied

Neurotoxic effect of acamprosate, n-acetyl-homotaurine, in cultured neurons.

Acamprosate (AC), N-acetyl-homotaurine, has recently been introduced for treating alcohol craving and reducing relapses in weaned alcoholics. AC may exert its action through the taurine system rather than the glutamatergic or GABAergic system. This conclusion is based on the observations that AC strongly inhibits the binding of taurine to taurine receptors while it has little effect on the binding of glutamate to glutamate receptors or muscimol to GABA(A) receptors. In addition, AC was found to be neurotoxic, at least in neuronal cultures, triggering neuronal damage at 1 mM. The underlying mechanism of AC-induced neuronal injury appears to be due to its action in increasing the intracellular calcium level, [Ca2+](i). Both AC-induced neurotoxicity and elevation of [Ca2+](i) can be prevented by taurine suggesting that AC may exert its effect through its antagonistic interaction with taurine receptors.

Acamprosate↗
PubMedDate not supplied

Computed tomography of gastrocolic ligament: involvement in malignant tumors of the stomach.

BACKGROUND: This study investigated computed tomographic (CT) features and anatomic bases of gastrocolic ligament involvement in malignant neoplasms of the stomach. METHODS: We retrospectively reviewed CT scans of 34 patients known to have gastric malignant neoplasm and gastrocolic ligament involvement. Emphasis was placed on direct invasion, lymph node metastasis, and omental seeding. RESULTS: CT manifestations of gastrocolic ligament involvement included direct invasion (38.2%, 13 of 34), enlargement of lymph nodes (50%, 17 of 34), "smudged" appearance (26.5%, nine of 34), "omental caking" (5.9%, two of 34), cystic mass (2.9%, one of 34), and varices of the omentum (2.9%, one of 34). We also found that gastric carcinoma and gastrointestinal stromal tumor invaded the transverse colon through the gastrocolic ligament in six patients (17.6%, six of 34). CONCLUSION: CT scan is useful for detecting gastrocolic ligament involvement in gastric malignant neoplasm. The imaging features consist of a mass sign, enlargement of lymph nodes, smudged appearance, omental caking, and so on. Gastric malignant neoplasm also may involve the transverse colon through the gastrocolic ligament.

Adenocarcinoma↗