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Biomedical subjects

J Shan

Publications and source records attributed to J Shan.

65 records · Page 4Linked to original sources
PubMed1994

Clinical aspects of parathyroid hypertensive factor.

Parathyroid hypertensive factor (PHF) in rats: PHF is an endogenous hypertensive substance which was originally associated with hypertension in spontaneously hypertensive rats (SHR). In this model, PHF was shown to act by increasing intracellular calcium levels in vascular smooth muscle and was linked with a characteristic pattern of abnormalities in overall calcium regulation. The action of PHF was blocked by calcium antagonists, suggesting that the effect of PHF was to increase extracellular calcium uptake. In SHR the parathyroid glands were shown to be the site of PHF secretion. This secretion was inhibited by an increase in dietary calcium. PHF was further shown to be unique to low-renin forms of hypertension, that is, those forms of hypertension characterized by abnormalities in calcium metabolism. PHF in humans: PHF was subsequently found in human low-renin salt-sensitive hypertension. As in SHR, calcium supplementation can lower PHF levels in humans. Similarly, there is circumstantial evidence for the parathyroid origin of PHF in humans. In human hypertensive patients, the presence of PHF has been shown to predict a favorable therapeutic response to calcium channel blockade. Recently, many of the abnormalities in calcium metabolism present in low-renin hypertension have also been described in other disease states. Notable among these diseases is non-insulin dependent diabetes mellitus. A survey of human non-insulin dependent diabetes mellitus has revealed that PHF was present in a disproportionate number of these patients independently of the blood pressure level. The significance of this latter finding needs to be explored, but PHF may prove to have relevance in diseases other than hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Human parathyroid hormone fragment(1-34) and human [Ala25,26,27]parathyroid hormone fragment(1-34): their vascular and intracellular calcium regulating action in vascular smooth muscle cells.

Human parathyroid hormone fragment, hPTH(1-34) and its analog, [Ala25,26,27]hPTH(1-34), were tested for their effects on rat blood pressure, tension generation in rat tail artery helical strips and intracellular calcium concentration ([Ca++]i) in smooth muscle cells of the rat tail artery. Amino acids at positions 25, 26 and 27 are reported to be responsible for the vascular action of the PTH molecule. The present studies demonstrate that hPTH(1-34), but not [Ala25,26,27]hPTH(1-34), produces a dose-dependent hypotensive effect in Sprague-Dawley (SD) rats and a dose-dependent relaxing effect on SD rat tail artery helical strips precontracted by norepinephrine, KCl or arginine vasopressin. Accordingly, hPTH(1-34), but not [Ala25,26,27]hPTH(1-34), inhibits the [Ca++]i increment induced by 15 mM KCl in cultured vascular smooth muscle cells (VSMC) from the SD rat tail artery after incubation with the peptide for 5 to 10 min. In addition, both hPTH(1-34) and [Ala25,26,27]hPTH(1-34) cause an initial transient and immediate increase in [Ca++]i in VSMC which does not correlate with any demonstrable vascular action. We suggest that PTH can elicit an initial increase in [Ca++]i and a subsequent inhibition of stimulated [Ca++]i increase in VSMC. The initial [Ca++]i effect is not related to its vascular action, whereas the subsequent inhibitory effect correlates well with its hypotensive effect.

Alanine↗
PubMed1993

1,25-dihydroxyvitamin D as a cardiovascular hormone. Effects on calcium current and cytosolic free calcium in vascular smooth muscle cells.

Clinical and in vitro evidence suggests a role for the calcium regulating hormone, 1,25-dihydroxyvitamin D (1,25D) in human and experimental hypertension. To establish the cellular basis for this association, we utilized the whole-cell version of the patch clamp method and fluorescence spectroscopic techniques to measure voltage-dependent calcium channel activity and cytosolic free calcium concentrations ([Ca2+]i) in rat tail artery-derived smooth muscle cells, before and after the addition of 1,25D. 1,25D significantly increased the calcium channel current over the range of test pulses, from -40 to +60 mV, in a dose- and time-dependent manner, appearing by 5 to 10 min of exposure, with maximum effects by 15 min. At 10 and 30 nmol/L, the current increased to 149 +/- 10% and 221 +/- 13% of basal activity of 37.75 +/- 7.7 pA and 37.7 +/- 4.5 pA, respectively. Similarly, at 10 and 100 nmol/L, 1,25D increased cytosolic free calcium levels 115 +/- 2% and 171 +/- 11%, from basal values of 99 +/- 32 nmol/L and 116 +/- 10 nmol/L, respectively. These effects of [Ca2+]i developed slowly over 3 to 4 min. Peak values were achieved by 30 min of incubation and were reversible with removal of 1,25D from the medium. Altogether, these direct effects of 1,25D on calcium current and [Ca2+]i in vascular smooth muscle cells support a role for 1,25D in vascular physiology, and provide a cellular basis for better understanding the involvement of 1,25D in hypertensive vascular disease.

Animals↗
PubMed1992

Parathyroid function in hypertension.

PHF, secreted by the PTG, induces hypertension by increasing vascular smooth muscle calcium uptake and thereby increasing intracellular calcium levels. PHF secretion is inhibited by dietary calcium and the effects of PHF are blocked by calcium channel antagonists. This explains the paradox whereby both calcium and calcium channel blockers may be effective antihypertensive agents. PHF may be secreted by a specific cell type in the parathyroid gland, numbers of which seem to correlate with PHF levels. Thus, the parathyroid gland does seem to play a role in some forms of hypertension, but this role is probably not due to its production of PTH, but may be related to the secretion of the new factor--PHF.

Animals↗
PubMed1990

Control of calcium channels in neuroblastoma cells (N1E-115).

Neuroblastoma cells (N1E-115) were used as models of transient (T) and long-lasting (L) Ca++ channels. The whole cell version of the patch clamp technique was used to measure inward Ca++ currents, and the fluorescent indicator, Fura-2, was used to measure changes in intracellular Ca++. Cells were cultured and selected during recording so that predominantly T or L channel currents were measured. T channel currents did not respond to dihydropyridine or parathyroid hormone, whereas L channel currents did. BAY-K-8644 increased and nifedipine decreased L channel currents. After a 15 mM KCl challenge, cells with predominantly T channels responded with a transient change in intracellular Ca++, while cells with predominantly L channels showed a sustained response. PTH inhibited the increase in intracellular Ca++ in cells with L channels, but not in those with T channels. PTH may be an example of an endogenous calcium channel blocker, at least in neuroblastoma cells.

Calcium Channel Blockers↗
PubMed1990

Specific inhibition of long-lasting, L-type calcium channels by synthetic parathyroid hormone.

The effect of an active synthetic N-terminal fragment of bovine parathyroid hormone (bPTH), bPTH-(1-34), on Ca2+ channels was studied in mouse neuroblastoma cells (N1E-115). With the whole-cell variation of the patch-clamp technique, T (transient) and L (long-lasting) types of Ca2+ currents were identified. Pharmacological characterization showed that the L current was amplified by the Ca2+ channel stimulator BAY K-8644, but the T current was unaffected. The administration of bPTH-(1-34) produced dose-related inhibition of the L current, which could be reversed by BAY K-8644. The peptide had no effect on the T current. In addition, use of the fluorescent indicator fura-2 showed that bPTH-(1-34) inhibited the KCl-stimulated increase in intracellular free Ca2+ in neuroblastoma cells with L channels but not in cells with T channels. An inactivated (oxidized) preparation of bPTH-(1-34) failed to affect the L current. High-affinity binding of labeled PTH analog to these neuroblastoma cells was also demonstrated. In addition, bPTH-(1-34) inhibited the L current in cultured vascular smooth muscle cells from rat tail artery. These data indicate that, in some tissues, PTH can act as an endogenous blocker of Ca2+ entry.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1990

[Induced labor for gravidae with low Bishop's scores (with report of 242 cases)].

In planned/selective delivery, gravidae with Bishop's score 5 or below 5 are deal with lower position water sac, the aim of which is to induce regular uterine contraction and complete physiological latent period of cervical dilation. From Oct 1986 to Dec 1988, 242 cases of primiparae by this method and the latent period in physiological limit. This is a great breakthrough in induced labour for gravidae with low Bishop's scores. We found that this method is simple, effective, safe, and economic. It not only alleviates pain of the gravidae, but also helps to prevent the rise of caesarean section rate.

Cervix Uteri↗
PubMedDate not supplied

Modulation of sympathetic actions on the heart by opioid receptor stimulation.

The sympathetic nervous system, the most important extrinsic regulatory mechanism of the heart, is inhibited postsynaptically and presynaptically by opioid peptides produced in the heart via their respective receptors. The cardiac actions of beta-adrenergic receptor (beta-AR) stimulation are attenuated by activation of the opioid receptor (OR) with OR agonist at ineffective concentrations, implying cross-talk between the OR and beta-AR. This cross-talk results from inhibition of the Gs protein and adenylyl cyclase of the beta-AR pathway by the pertussis toxin-sensitive G protein of the opioid pathway. Alterations in cross-talk between these two receptors occur in pathological situations to meet bodily needs. In myocardial ischemia, when the sympathetic activity is increased, the inhibition of beta-AR stimulation by kappa-opioid stimulation is also enhanced, thus reducing the workload, oxygen consumption and cardiac injury. Whereas cardiac responsiveness to sympathetic discharges is also reduced after chronic hypoxia, the cross-talk between kappa-OR and beta-AR is reduced to prevent undue suppression of the sympathetic influence on the heart. On the other hand, impairment of the cross-talk may result in abnormality. A lack or a significant reduction in the inhibition of beta-AR stimulation by kappa-OR stimulation may lead to an excessive increase in cardiac activities, which contribute to the maintenance of high arterial blood pressure in spontaneously hypertensive rats. Other than opioid peptides, female sex hormone and adenosine also inhibit the sympathetic actions on the heart. In addition, sympathetic action is also inhibited presynaptically by kappa-opioid peptides via their receptor.

Animals↗