Regulation of parathyroid hypertensive factor secretion by vitamin D3 analogs in parathyroid cells derived from spontaneously hypertensive rats.

Parathyroid hypertensive factor (PHF) is a novel substance secreted by the parathyroid gland (PTG), which is elevated in 30-40% of all hypertensive patients; specifically, the low-renin subset. However, very little is known about the regulation of PHF secretion. Since the classical parathyroid regulator, 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3), may be elevated concurrent with or preceding the development of low-renin hypertension and elevated plasma PHF, we hypothesized that 1,25-(OH)2D3 would stimulate PHF release.

The role of Ca2+ channel modulation in the neuroprotective actions of estrogen in beta-amyloid protein and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) cytotoxic models.

Physiologically relevant concentrations of 17beta-estradiol (E2) are neuroprotective in both beta-amyloid protein 25-35 (Abeta) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced cytotoxicity in SK-N-SH cells. MPTP, but not Abeta, induces apoptosis in this cell line. The L-type calcium channel blocker nifedipine or decreased extracellular Ca(2+) concentration blocked Abeta-induced cell death, but not MPTP-induced cell death.

Regulation of parathyroid hypertensive factor secretion by Ca2+ in spontaneously hypertensive rat parathyroid cells.

Background: Elevated parathyroid hypertensive factor (PHF) has been suggested to play a causal role in the pathogenesis of hypertension. Previous studies have indicated that PHF secretion is stimulated by low extracellular (EC) Ca2+. Therefore, we hypothesized that the calcium-sensing receptor (CaR) is involved in regulation of PHF release.

Protein kinase C masks nitric oxide synthase activity in vascular smooth muscle under basal conditions.

Under basal conditions there is no observable nitric oxide synthase (NOS) activity in vascular smooth muscle (VSM). Pretreatment of endothelium-denuded aortic rings from Sprague-Dawley rats with 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7), (0.1 micromol/L) significantly attenuated phenylephrine (PE)-induced contractile responses in a dose-dependent manner.

The neuroprotective effects of estrogen in SK-N-SH neuroblastoma cell cultures.

Estrogen has been considered to be a neuroprotectant and a neuromodulator in many neuronal cell lines and tissue preparations. The protective effects of estrogen may be mediated through classical estrogen receptors (ERs), or may be due to its anti-oxidant properties which are independent of receptors. The current studies show that 17beta-estradiol (E2) is neuroprotective against beta-amyloid protein 25-35 (Abeta)-, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-, high density culture condition-, and serum deprivation-induced neuronal death in SK-N-SH human neuroblastoma cells.

Gamma-dendrotoxin blocks large conductance Ca2+-activated K+ channels in neuroblastoma cells.

In N1E 115 neuroblastoma cells, gamma-dendrotoxin (DTX, 200 nM) blocked the outward K(+) current by 31.1 +/- 3.5% (n = 4) with approximately 500 nM Ca(2+) in the pipet solution, but had no effect on the outward K(+) current when internal Ca(2+) was reduced.

The establishment of a reliable cytotoxic system with SK-N-SH neuroblastoma cell culture.

A reliable in vitro cytotoxic system is essential in neurocytotoxic and neuroprotective research. The present study examined four cytotoxic insults with the SK-N-SH human neuroblastoma cell line. These were beta-amyloid protein (Abeta), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), high density culture, and serum deprivation induced neuronal death.

Rapid inhibition of the contraction of rat tail artery by progesterone is mediated by inhibition of calcium currents.

Progesterone induced rapid relaxation of KCl-contracted tail artery helical strips from rats. The effect was dose dependent, with an IC50 (inhibitory concentration which produces 50% of the maximal response) of 8.9 microM progesterone.

Rapid effect of progesterone on the contraction of rat aorta in-vitro.

Progesterone induced rapid relaxation of KCl-induced contraction of rat aortic rings. The relaxant effect of progesterone on aortic rings was concentration-dependent (over the range of 10(-10) to 10(-5) M) and partially dependent on the endothelium. Application of a nitric oxide (NO) synthase antagonist N(G)-monomethyl-L-arginine (L-NMMA, 10(-5) M) after progesterone treatment partially inhibited the relaxant effects of progesterone.

Problems in the use of herbal and natural substances, with a specific example concerning the cardiovascular system.

1. There has been increasing awareness and use of natural preparations for health purposes by consumers. 2.

Neurotrophic and neuroprotective actions of ginsenosides Rb(1) and Rg(1).

The ginsenosides have many pharmacological actions, including various actions on the nervous system. Our previous studies have demonstrated that two ginsenosides, Rb(1) and Rg(1) improve performance in a passive avoidance-learning paradigm and enhance cholinergic metabolism. The present study was designed to examine the cellular neurotrophic and neuroprotective actions of two pure ginsenosides in two model systems.

Effect of the herbal extract combination Panax quinquefolium and Ginkgo biloba on attention-deficit hyperactivity disorder: a pilot study.

Objective: A combination herbal product containing American ginseng extract, Panax quinquefolium, (200 mg) and Ginkgo biloba extract (50 mg) (AD-FX; CV Technologies, Edmonton, Alta.) was tested for its ability to improve the symptoms of attention-deficit hyperactivity disorder (ADHD).

Design: Open study.

Quantitative determination of parathyroid hypertensive factor by enzyme-linked immunosorbent assay.

A new competitive enzyme immunoassay for the detection parathyroid hypertensive factor (PHF) in human plasma using a PHF-horseradish peroxidase conjugate and IgM antibody adsorbed on the microtiter plate was established. The antibodies raised against rat PHF could recognize human PHF. Cross-reactivity of anti-PHF antibodies with other serum haptens and proteins was negligible.

Parathyroid hormone (PTH) and parathyroid hormone-related protein (PTHrP) relax cholecystokinin-induced tension in guinea pig gallbladder strips.

Parathyroid hormone (PTH) and parathyroid hormone-related protein (PTHrP) have been shown to relax various types of smooth muscle, e.g. vascular, uterine and gastric.

Parathyroid hypertensive factor secretion from subcultured spontaneously hypertensive rat parathyroid cells.

Cells dissociated from spontaneously hypertensive rat (SHR) parathyroid glands were grown in culture. Media harvested from the cell cultures were analyzed for parathyroid hypertensive factor (PHF) using the blood pressure bioassay. Cells raised in DMEM containing normal (1.

Parathyroid hypertensive factor inhibits voltage-gated K+ channels in vascular smooth muscle cells.

Parathyroid hypertensive factor (PHF) has been implicated in regulation of vascular smooth muscle tone and pathogenesis of several forms of hypertension. Earlier studies have suggested that PHF enhances the actions of other vasoconstrictors, while it has no in vitro vasoconstrictor property of its own. PHF was previously found to enhance the L-type Ca channel currents and intracellular Ca responses to depolarization in vascular smooth muscle cells (VSMCs).

American ginseng extract reduces scopolamine-induced amnesia in a spatial learning task.

Objective: To determine if HT-1001, an extract of American ginseng, affects scopolamine-induced memory and performance deficits in a spatial learning task, alters brain concentrations of aminergic neurotransmitters, and alters choline uptake in synaptosome preparations.

Design: Animal study.

Animals: 48 Sprague Dawley rats.

Prostaglandin E2 modulates a non-inactivating potassium current in rat neurohypophyseal nerve terminals.

A non-inactivating voltage dependent K+ channel current was observed in neuro-hypophyseal nerve terminals. This current was sensitive to inhibition by 4-aminopyridine and tetraethyl ammonium chloride, but was not sensitive to inhibition by alpha- or beta-dendrotoxin. Prostaglandin E2 (PGE2) modulated the voltage-dependent K+ channel, through a receptor-mediated process, as indicated by meclofenamate sensitivity, and this involved the activation of G protein(s), as indicated by sensitivity to guanosine-5'-O-(2-thiodiphosphate) (GDPfS).

Nitric oxide selectively inhibits intracellular Ca++ release elicited by inositol trisphosphate but not caffeine in rat vascular smooth muscle.

The present study was designed to investigate whether nitric oxide (NO) could interfere with intracellular Ca++ release through different pathways in vascular smooth muscle. Phasic contractions of rat aorta induced by phenylephrine or caffeine in Ca++-free solution were used as an indicator of intracellular Ca++ release through the inositol 1,4,5-triphosphate receptor pathway and the ryanodine receptor pathway, respectively. In addition, cytoplasmic Ca++ concentration ([Ca++]i) in vascular smooth muscle cells was determined by fluorescence measurement.

The actions of prostaglandin E2 on potassium currents in rat tail artery vascular smooth muscle cells: regulation by protein kinase A and protein kinase C.

In vascular smooth muscle cells (VSMCs) of rat tail artery, prostaglandin E2 (PGE2) inhibited a voltage-dependent, delayed rectifier K channel current (Ik). The inhibition was concentration-dependent, via a receptor-mediated mechanism involving the activation of G protein(s) (Ren et al., 1995).

Calcium mobilization and isometric tension in bovine tracheal smooth muscle: effects of salbutamol and histamine.

We determined if decreases in relative free intracellular calcium concentration ([Ca2+]i) caused by salbutamol, a selective beta2-adrenoreceptor agonist, were paralleled by calcium egression from the cytosol in bovine trachealis muscle strips. [Ca2+]i, or tissue-surface extracellular calcium changes (Ts[Ca2+]ext), were monitored using Fluo-3 acetoxymethylester or Fluo-3 pentaammonium salt simultaneously with isometric tension. Salbutamol (1 microM) decreased histamine-induced isometric tension from an average peak tension of 128.

Prostaglandin E2 contracts vascular smooth muscle and inhibits potassium currents in vascular smooth muscle cells of rat tail artery.

There is evidence to suggest that PGE2 plays an important role in the regulation of vascular smooth muscle tone. To determine the cellular basis of this action, we studied the effect of PGE2 on force in helical muscle strips from rat tail artery. PGE2 evoked a sustained contractile response.