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M C Yang

Publications and source records attributed to M C Yang.

At least 109 records · Page 6Linked to original sources
PubMed1990

Mechanisms of the vascular action of parathyroid hormone.

The vasodilatory effect of parathyroid hormone (PTH) has been investigated repeatedly and confirmed over the past few years. The present study correlates the PTH-induced vasodilatory effect with the biochemical changes in cyclic AMP (cAMP) content and Ca++ uptake in the vascular tissue. Synthetic fragment bPTH-(1-34) (1.2 X 10(-7) M) significantly inhibited the contraction of the isolated tail artery of rat induced by KCl (30-80 mM). It also relaxed KCl (40 and 60 mM)-induced contractions in a concentration-dependent manner [2.7 X 10(-9) to 3.7 X 10(-8) M)]. In addition, the concentration-contraction curve of Ca (0.3-3.0 mM) was shifted to the right by PTH in 40 mM KCl Krebs-Henseleit solution. These suggest the blocking effects of PTH on Ca entry. This hypothesis was supported by a study in which PTH inhibited KCl-enhanced 45Ca uptake, an effect similar to that of D600. In the experiment with matched tissue, PTH increased tissue cAMP content whereas KCl did not. These suggest that the vascular actions of PTH may involve both cAMP and Ca entry blocking. It is important to know that PTH was capable of stimulating cAMP content in Ca-free medium, suggesting that the increase in cAMP level by PTH may not be secondary to the change in Ca++ uptake.

Animals↗
PubMed1989

Effect of calcium diet on the vascular reactivity of DOCA-salt hypertensive rats.

It has been demonstrated that an increase in dietary calcium intake can lower the blood pressure of the hypertensives. We examined the effect of dietary calcium on blood pressure and vascular reactivity in DOCA-salt hypertensive rats. Blood pressure was significantly decreased after four weeks of calcium feeding. Nevertheless, the development of hypertension was not completely avoided. There was no difference between the calcium fed group and the control group in their response to NE, KCl and AVP in tail artery helical strips in normal calcium medium in vitro. However, the responses of these two groups to NE (10(-6) M) and AVP (10mU) were significantly different in Ca2+-free medium. Furthermore, the tail artery from Ca-fed group was less responsive to K+-induced relaxation. Since K+-induced relaxation has been applied to indicate the activity of Na+-K+ pump, we suggest that the activity of Na+-K+ pump may be involved and that the change in vascular reactivity to agonists might be rather insignificant in lowering the blood pressure of Ca-fed DOCA-salt hypertensive rats.

Animals↗
PubMed1989

Unsaturated fatty acids inhibit IL-2 production in thymus-dependent antibody responses in vitro.

Albumin-complexed unsaturated fatty acids such as oleic acid (18:1) exerted a dose-dependent inhibitory effect on in vitro primary anti-TNP plaque-forming cell (PFC) responses to trinitrophenyl keyhole limpet haemocyanin (TNP-KLH), but did not affect primary PFC responses to trinitrophenyl lipopolysaccharide (TNP-LPS). The addition of 150 microM 18:1 at the initiation of thymus-dependent (T-D) antibody cultures inhibited the subsequent PFC response by 85%, and removal of the fatty acid after 24 hr did not reverse its inhibitory effect. By contrast, delaying the addition of 18:1 until 3 or 4 days after culture initiation abrogated its inhibitory effects. T-D antibody cultures displayed maximum production of interleukin-2 (IL-2) on the third day after culture initiation and a 24-hr exposure to 18:1 resulted in a dose-dependent inhibition of IL-2 production. Lastly, the addition of exogenous IL-2 reversed the inhibition of PFC responses in cultures transiently exposed to 18:1. These findings suggest that unsaturated fatty acids inhibit in vitro T-D PFC responses by selectively interfering with early stages of the antibody response, particularly those events leading to IL-2 production by T-helper cells.

Animals↗
PubMed1988

Parathyroid hormone and calcium entry blockade in a vascular tissue.

The mechanism of the vasorelaxing action of a synthetic parathyroid hormone fragment, bPTH-(1-34), was studied. Rat tail artery helical strips were constricted in vitro with potassium chloride (6 x 10(-2) M), arginine vasopressin (2 mU/ml) or BAY-K-8644 (3 x 10(-7) M in the presence of 1.5 x 10(-2) M KCl). bPTH-(1-34) was able to relax the constricted tissue or to inhibit the constriction. All three constricting agents increased calcium uptake by the vascular tissue as determined by the measurement of the low-affinity lanthanum-resistant pool of calcium. Such increases in calcium uptake were significantly reduced by bPTH-(1-34). These data suggest that PTH may be a natural circulating hormone or chemical capable of inhibiting calcium entry in a vascular tissue.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1988

Local suppressive effect of clonidine on penile erection in the dog.

Dogs, 8.5 to 10 kg. in weight, were anesthetized with sodium pentobarbital (35 mg./kg.), intraperitoneally. Penile erection as indicated by an increase in the intracorporal pressure (ICP-increase) was produced by electrical stimulation of the right cavernous nerves. Drugs were administered into the internal pudendal artery (IPA) and femoral vein. A low dose (0.2 to 0.4 microgram/kg.) of clonidine, an alpha 2 adrenoceptor agonist, which could not affect either ICP or systemic arterial pressure (SAP) through an intravenous route, did suppress the ICP-increase markedly via direct injection into the IPA which supplies the penile blood flow. By intra-IPA injection, yohimbine (2.5 micrograms/kg.), an alpha 2 adrenoceptor antagonist, remarkably restored the ICP to the erection state. By intravenous injection, clonidine at a dose of 1.6 to 3.2 micrograms/kg. also profoundly reduced the ICP-increase, but only negligibly lowered the SAP. The IPA blood flow (IPAF) decreased coincidentally when the ICP-increase was effectively reduced by either intravenous or intra-IPA injection of clonidine. These findings suggest clonidine could act locally in the penile structure to suppress penile erection, possibly resulting from a penile vasoconstriction involving alpha 2 adrenoceptor. Whether this vasoconstriction is caused by a direct alpha 2 stimulating effect on the vascular smooth muscle or by an alpha 2 presynaptic inhibition of the vasodilator nerve (cavernous nerve) endings has been discussed.

Animals↗
PubMed1987

Structure-activity relationship of parathyroid hormone: relative sensitivity of rabbit renal microvessel and tubule adenylate cyclases to oxidized PTH and PTH inhibitors.

It has been shown previously that secondary structural changes of bPTH-(1-34) (synthetic amino-terminal (1-34) fragment of bovine parathyroid hormone), obtained by oxidation of the methionines 8 and 18, abolished its hypotensive but not its hypercalcemic action. Hence, it has been postulated that the various physiological effects of the hormone are mediated by different receptors that require different regions or configurations of the peptide. To further examine this hypothesis the relative sensitivity of the PTH-responsive adenylate cyclase of microvessels and tubules isolated from rabbit kidney cortex, to oxidized PTH and PTH inhibitors, was examined. In the presence of GTP, bPTH-(1-34) stimulated both microvessel and tubule adenylate cyclase in a dose-dependent fashion and with analogous affinities (ED50 = 52 nM in the microvessels and 85 nM in the tubules). Hydrogen peroxide treatment of bPTH-(1-34) resulted in the loss of the adenylate cyclase stimulating potency in the microvessels while there was substantial enzyme activation (ED50 = 900 nM) in the tubules. Oxidized PTH inhibited the untreated PTH-stimulated adenylate cyclase, suggesting that oxidized PTH still retains an affinity for vascular receptor sites. Similar treatment of the sulfur-free PTH analog [Nle8,18, Tyr34]bPTH-(1-34)NH2, where methionines have been replaced by norleucine, had little or no effect in both fractions. In the microvessels the synthetic PTH antagonist analogs [Nle8,18, Tyr34]bPTH-(3-34)NH2 and [Tyr34]bPTH-(7-34)NH2, strongly inhibited the adenylate cyclase responses to bPTH-(1-34). No inhibition was seen in the tubules with the same molar ratios of inhibitor to native PTH. Together, these results suggest strongly that the differences in the adenylate cyclase response to various PTH fragments most likely represent a difference in the structural requirements for PTH actions between microvessels and tubules.

Adenylyl Cyclases↗
PubMed1987

Protein and metabolizable energy requirements of hand-fed squabs from hatching to 28 days of age.

Incubator-hatched squabs were hand fed slurries containing 14% diet and 86% water by weight for the 1st 4 days, followed by 20% diet and 80% water for the next 2 to 3 days. From Days 7 to 28, the slurry contained 25% diet and 75% water. A diet containing about 61% isolated soybean protein, 8.9% soybean oil, 21.5% glucose, 4% CaHPO4.2H2O, and 1.3% CaCO3 supplemented with vitamins and trace elements supported the optimum growth of squabs for the first 7 days. It contained 3,675 kcal metabolizable energy (ME)/kg and 53.3% crude protein (CP). The composition of the optimum diet for feeding from Days 7 to 289 was as follows: corn starch, 58.37%; isolated soybean protein, 23.1%; cellulose, 8.0%; soybean oil, 3.0%; CaHPO4.2H2O, 3.0; methionine, .3%; CaCO3, 1.0; plus vitamins and trace minerals. This diet provided 3,200 kcal ME/kg and 20% CP.

Aging↗
PubMed1987

Hemodynamic effects of bPTH(1-34) and its analogue Nle8,18Tyr34bPTH(3-34) amide.

We examined the vascular effects of bovine PTH(1-34) and of an analogue, Nle8,18Tyr34bPTH(3-34) amide, which inhibits adenylate cyclase activation by bPTH(1-34) in a number of in vitro systems. In the conscious dog. bPTH(1-34) injection produced dose-dependent hypotension associated with increased heart rate and cardiac output. The (3-34) analogue had no hypotensive effect in doses up to 6.0 micrograms/kg (1.5 nM/kg). In vitro studies revealed that bPTH(1-34) relaxed pitressin-contracted helical strips from the rat caudal artery. The (3-34) analogue displayed a weak, but definite inhibitory effect against the vasorelaxant effects of bPTH(1-34) with a pA2 of 5.5. The results further characterize the previously established hypotensive and vasorelaxant actions of bPTH(1-34), and suggest that the (3-34) analogue, which inhibits adenylate cyclase generation by bPTH(1-34) in nonvascular tissues, antagonizes the vasorelaxant effects of bPTH(1-34) as well. The results provide suggestive evidence that the vasorelaxant effects of bPTH(1-34) may be mediated by adenylate cyclase.

Animals↗
PubMed1986

Kinetics of membrane immunoglobulin capping on murine B lymphocytes. Effects of phospholipid fatty acid replacement.

Detailed analyses regarding the effects of temperature and phospholipid fatty acid replacement on the capping of membrane immunoglobulin (mIg) have been performed using a recently described flow cytometric procedure (Cuchens, M. A., and Buttke, T. M. (1984) Cytometry 5, 601-609). Purified murine B cells were incubated for 12-20 h in the presence of bovine serum albumin-complexed 80 microM stearic (18:0), oleic (cis-18:1), or linoleic (cis, cis-18:2) free fatty acids. Unmodified and free fatty acid-treated cells were stained with fluorescein-conjugated rabbit anti-mouse Ig and subjected to pulse-shape (width) analyses to follow the kinetics of mIg capping. In both unmodified and free fatty acid-treated cells, capping of mIg occurred at all temperatures between 17 and 37 degrees C, but the rate of cap formation was temperature dependent. Arrhenius plots of mIg capping were linear, with activation energies ranging from 14 to 23 kcal/mol depending on the saturated/unsaturated fatty acid ratio of B cell phospholipids. Ligand-induced redistribution of mIg thus appears to be sensitive to changes in membrane acyl chain composition.

Animals↗
PubMed1986

Cyclic AMP and the vascular action of parathyroid hormone.

The involvement of tissue cAMP in the vasodilating action of parathyroid hormone (PTH) was investigated. The bovine active fragment bPTH-(1-34) was used in all studies. In anesthetized dogs, theophylline, a phosphodiesterase inhibitor, potentiated the hypotensive action of bPTH-(1-34) at the dose of 1 microgram/kg. The potentiation was related to the dose of theophylline infused. In an in vitro rat tail artery helical strip assay, dibutyryl cAMP produced dose-related relaxation in arginine vasopressin (AVP) constricted blood vessels. bPTH-(1-34) also produced dose-related relaxation in the tail artery constricted by AVP. In the presence of isobutylmethylxanthine, another phosphodiesterase inhibitor, the bPTH-(1-34) dose--response curve was shifted to the left, indicating potentiation. Imidazole, which has phosphodiesterase stimulating activity, significantly decreased the in vitro vasorelaxing effect of bPTH-(1-34). In addition, bPTH-(1-34) increased significantly the rat tail artery cAMP content. b-PTH-(1-34) oxidized with hydrogen peroxide lost its vasorelaxing activity and was also ineffective in increasing the tail artery cAMP content. All these data strongly suggest that cAMP may be involved in eliciting the vasorelaxing action of bPTH-(1-34).

1-Methyl-3-isobutylxanthine↗
PubMed1985

The vasorelaxant action of parathyroid hormone fragments on isolated rat tail artery.

Previous studies have demonstrated that parathyroid hormone (PTH) and its 1-34 amino terminal fragment possess a hypotensive action in vivo which appeared to be direct and dose-dependent. However, attempts to demonstrate the phenomenon in isolated vascular tissue have been minimally successful at best. The present study reports that bovine PTH-(1-34) can relax isolated rat tail artery helical strips precontracted by either arginine vasopressin, depolarizing concentrations of potassium chloride, or norepinephrine. The phenomenon occurs in a dose-dependent manner and is not dependent upon the presence of the endothelial lining of the vessels. These studies support the hypothesis that bovine PTH-(1-34) produces a direct vasorelaxant action mainly in small arteries.

Animals↗
PubMed1984

Hypotensive action of parathyroid hormone in chicken.

In a recent series of studies, the hypotensive action of parathyroid hormone (PTH) was demonstrated in several vertebrate species. In mammals, the mechanism of this direct action on specific vascular beds was studied. An increase in intracellular cyclic AMP and an inhibition of entry of extracellular calcium into the vascular tissue was correlated with the vasorelaxing action of PTH. In the present report, PTH was found to relax chicken mesenteric vessels in vitro in the presence or absence of constriction with concentrated potassium chloride (KCl). PTH produced dose-related inhibition of the chicken vessel constricted with 10, 20, 40, or 60 mM KCl. Extracellular calcium-dependent constriction of the chicken mesenteric artery was also decreased by PTH. An inhibitory effect was also observed with D600, a known calcium-entry inhibitor, in the above in vitro test systems. The low affinity lanthanum-resistant pool of calcium, which supposedly reflects the rate of calcium entry into cells, was also decreased by PTH in the control or KCl-stimulated chicken mesenteric artery. These data suggest that PTH may produce vasorelaxation in chicken mesenteric artery by inhibition of calcium entry into cells. This vessel from the chicken seems to have a high turnover rate of calcium and may be a good model for studying the effects of substances on calcium entry in vascular smooth muscle.

Animals↗