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PubMed1996

Role of calmodulin and myosin light-chain kinase in lung ischemia-reperfusion injury.

It is generally accepted that microvascular permeability is controlled by intercellular endothelial cell gap size. This process is controlled in endothelial cell monolayers and peripheral blood vessels by calmodulin (CaM)-dependent myosin light-chain kinase (MLCK), which phosphorylates MLC20 with subsequent actin-myosin interaction. In the present study both CaM and MLCK blockers were studied during ischemia-reperfusion (I/R)-induced injury in isolated buffer-perfused rat lungs. The effects of a calcium ionophore (CaI) were tested in isolated intact rat lungs to compare the effects of increasing intracellular Ca2+ to I/R-induced damage. Because protein kinase C (PKC) could also be a mediator of I/R injury, a PKC inhibitor was studied in lungs subjected to either I/R or CaI. In lungs subjected to I/R alone, a fivefold increase in microvascular permeability occurred after 30 min of reperfusion (P < 0.001), and a tenfold increase was present after an additional 60 min of reperfusion (P < 0.01). Pretreatment of the I/R lungs with a CaM inhibitor (trifluoperazine, 100 microM) or with a MLCK inhibitor (ML-7,500 nM) blocked the microvascular damage at both 30 and 90 min of reperfusion. When the CaM inhibitor was introduced into the venous reservoir after 46 min of reperfusion, after the microvascular damage was present, no further increase in microvascular permeability occurred. Pretreatment of the lungs with a PKC inhibitor (staurosporine, 100 nM) did not alter the magnitude of the increased microvascular permeability produced by I/R or the time course of the damage. The calcium ionophore A23187 (7.5 microM) caused increases in Kfc values similar to those produced by I/R. Pretreatment of A23187-treated lungs with a CaM inhibitor produced no protective effect on the microvascular injury at 30 min after administration. Pretreatment of the CaI-challenged lungs with staurosporine significantly increased the microvascular barrier injury at 30 min compared with that occurring with I/R. When a beta-adrenergic receptor agonist (isoproterenol, 10 microM) was introduced to the lung after CaI-induced damage had occurred, no further increase in microvascular permeability was observed, and a trend toward reversal of injury occurred. We conclude from these studies that CaM/MLCK/MLC20 system is involved in our model of I/R-induced rat lung injury but is not involved in lung injury associated with Ca2+ entering the cell.

Adrenergic beta-Agonists↗

PubMed1991

Mast cell degranulation in hemorrhagic shock in rats and the effects of vasoactive intestinal peptide, aprotinin and H1 and H2-receptor blockers on degranulation.

Various stressful stimuli cause mast cell degranulation. Hemorrhagic shock is one such stressful stimulus which may cause mast cell degranulation and histamine release. Histamine may be involved in the pathophysiology of hemorrhage. It was reported that there are large amounts of histamine in the anterior and posterior lobes of the pituitary and the adjacent median eminence of the hypothalamus. Most of the histamine in the posterior pituitary is in mast cells. In addition, both vasoactive intestinal peptide (VIP) and histamine-containing neurons are available in the hypothalamus. It therefore seems reasonable to suppose that these three systems (i.e., mast cells, VIP-containing neurons, and histamine-containing neurons) may play an important role in the progression of hemorrhagic shock. 66 albino rats (200-250 g) of either sex were used. The presence of mast cells was examined by light microscopy. Hemorrhage caused mast cell degranulation in a correlation with the amount of blood loss. In all cases, the most intense degranulation was observed in the hypothalamus, especially the nucleus arcuatus, and in the subcutaneous tissue. The intensity of degranulation gradually decreased in the peripheral blood vessel, peritoneum and omentum, in this order. VIP prevented degranulation, but aprotinin and H1 and H2 receptor blockers did not.

Animals↗

PubMed1989

Flow-mediated and reflex changes in large peripheral artery tone in humans.

Studies of peripheral blood vessels in humans have focused primarily on regulation of blood flow and vascular resistance, which are thought to reflect small vessel caliber. Recent studies in animals have identified flow-mediated and neurogenic changes in large artery diameter. This study tested for flow-mediated dilatation and reflex constriction of the brachial artery in humans. A dual-crystal pulsed Doppler system was used to measure brachial artery diameter and blood flow proximal to the antecubital fossa. To test for flow-mediated dilatation, flow through the brachial artery was altered by an occluding cuff placed on the forearm distal to the site of brachial artery flow and diameter measurement. Control blood flow was 123 +/- 20 ml/min, and brachial artery diameter was 4.74 +/- 0.17 mm (mean +/- SEM). By inflating the distal occluding cuff (distal circulatory arrest), flow was reduced through the brachial artery to 21 +/- 5 ml/min (p less than 0.005), and brachial artery diameter was reduced to 4.35 +/- 0.20 mm (p less than 0.001). By deflating the distal occluding cuff after 10 minutes (reactive hyperemia), brachial artery flow was increased to 358 +/- 55 ml/min (p less than 0.001), and diameter was increased to 5.6 +/- 0.19 mm (p less than 0.001). These interventions did not change systemic arterial pressure and, as measured in three subjects, caused only small changes in local brachial artery distending pressure. Thus, both increased and decreased brachial artery blood flow produced significant changes in brachial artery diameter without altering arterial distending pressure. These data provide evidence for flow-mediated dilatation in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1998

Central vagotonic effects of atropine modulate spectral oscillations of sympathetic nerve activity.

BACKGROUND: Low-dose atropine causes bradycardia either by acting on the sinoatrial node or by its effects on central muscarinic receptors increasing vagal activity. Any central muscarinic effects of high-dose atropine on RR interval are masked by peripheral muscarinic blockade at the sinoatrial node, which causes tachycardia. Effects of central parasympathetic activation on sympathetic activity are not known. METHODS AND RESULTS: Using power spectral analysis of RR interval, intra-arterial blood pressure, respiration, and muscle sympathetic nerve activity (MSNA), we examined the effects of both low (2 microgram/kg IV) and high (15 microgram/kg IV) doses of atropine. After low-dose atropine, RR increased by 9+/-1% (P<0.0001), the low-frequency (LF) component (in normalized units, NU) of RR variability decreased by -32+/-8%, and the high-frequency (HF)NU component increased (+74+/-19%); hence, LF/HF of RR variability fell by 52+/-10% (all P<0.01). Although overall MSNA did not change, LFNU of MSNA decreased (-15+/-5%), HFNU of MSNA increased (+31+/-3%), and LF/HF of MSNA fell (-41+/-8%) (all P<0.01). After high-dose atropine, LFNU of MSNA decreased (-17+/-12%), HFNU of MSNA increased (+22+/-3%), and LF/HF of MSNA fell (-51+/-21%) (all P<0.02). CONCLUSIONS: Increasing central parasympathetic activity with low-dose atropine is associated with an increase in the HF and a decrease in the LF oscillations of both RR interval and MSNA variability. High-dose atropine similarly induces an increase in the HF and a decrease in the LF components of MSNA variability. Thus, central parasympathetic activation is able to modulate the oscillatory characteristics of sympathetic nerve traffic to peripheral blood vessels.

Adult↗

PubMed2006

Sustained normalization of high blood pressure in spontaneously hypertensive rats by implanted hemin pump.

Treatment of established hypertension, especially for prolonged control of this pathogenic process, represents a great challenge. To upregulate the expression of heme oxygenase (HO) to lower blood pressure (BP) of spontaneously hypertensive rats (SHRs), we administered hemin to 12-week-old adult SHRs through subcutaneously implanted osmotic minipumps for 3 consecutive weeks (the hemin protocol). Systolic BP of SHRs was normalized 123+/-2 mm Hg (n=20; P<0.001) and this normalization maintained for 9 months after the removal of hemin pumps. At the end of the hemin protocol, HO-1 expression, HO activity, soluble guanylyl cyclase expression, and cGMP content were all increased, but phosphodiesterase-5 expression was downregulated in the mesenteric arteries. The hemin protocol also reversed SHR-featured arterial eutrophic inward remodeling and decreased expression levels of vascular endothelial growth factor. These changes lasted 9 months after the hemin protocol. Our study, thus, formulates a novel hemin protocol that will not only normalize BP in SHRs with established hypertension but, more importantly, will also provide long-lasting antihypertension protection. Sustained upregulation of HO-1-linked signaling pathways and reversal of vascular remodeling in peripheral blood vessels mediate likely the antihypertensive effect of the hemin protocol.

3',5'-Cyclic-GMP Phosphodiesterases↗

PubMed1992

Expression of alpha-smooth muscle actin in the developing kidney vasculature.

To determine whether alpha-smooth muscle (alpha-SM) isoactin is expressed in the maturing kidney as well as the changes associated with maturation, we processed for immunocytochemistry kidney sections from Wistar-Kyoto rats at various prenatal (15, 17, 19, and 20 days) and postnatal (2, 5, 10, 15, and 90 days) ages using a monoclonal anti-alpha-SM actin antibody. At 15 days of gestation, only a few mesenchymal cells contained alpha-SM actin. However, other fetal vasculature structures (heart, aorta, peripheral blood vessels) expressed alpha-SM actin. Vascular localization was first observed at 17 days of gestation in larger corticomedullary vessels. As maturation progressed, actin expression accompanied the outward growth and branching of the kidney vasculature. During fetal life (17 days), alpha-SM actin also was expressed within juxtamedullary glomeruli. As the centrifugal maturation of nephrons proceeded, intraglomerular expression extended to outer cortical glomeruli. After 10 days of postnatal life, once glomerular development was completed, intraglomerular expression was no longer present. Peritubular capillaries expressed alpha-SM actin during early (fetal and neonatal) development, but not in the adult kidney. We conclude that 1) expression of alpha-SM actin in the developing kidney is delayed with respect to other vascular beds, 2) expression of alpha-SM actin follows the centrifugal pattern of nephrovascular development, and 3) glomerular and peritubular capillary expression of alpha-SM actin is a transient developmental phenomenon associated with active glomerulogenesis and capillary growth.

Actins↗

PubMed1993

Calcitonin gene-related peptide gene expression in the spontaneously hypertensive rat.

Calcitonin gene-related peptide, a product of the calcitonin gene, is a potent vasodilator neuropeptide. We have demonstrated that dietary calcium deficiency decreased the neuronal (laminae I/II of the dorsal horn of the spinal cord) content of immunoreactive calcitonin gene-related peptide in the normal rat. Neuronal calcitonin gene-related peptide levels are also reduced in the spontaneously hypertensive rat, a model characterized by calcium deficiency. However, the mechanism of this reduction in neuronal calcitonin gene-related peptide could be due to decreased synthesis or increased release. To determine if neuronal calcitonin gene-related peptide messenger RNA (mRNA) levels are also decreased in the spontaneously hypertensive rat, we measured relative calcitonin gene-related peptide mRNA levels (using a genomic hybridization probe specific for alpha- and beta-calcitonin gene-related peptide mRNA) in dorsal root ganglia from spontaneously hypertensive and Wistar-Kyoto control rats. Dorsal root ganglia neuronal cell bodies are a prominent site of calcitonin gene-related peptide synthesis and send axons to peripheral blood vessels and central spinal cord sites (laminae I/II). After normalization of calcitonin gene-related peptide mRNA levels of 18S RNA, the calcitonin gene-related peptide mRNA/18S RNA ratio was significantly decreased approximately threefold in the spontaneously hypertensive rats compared with controls. This alteration in calcitonin gene-related peptide mRNA levels is specific for dorsal root ganglia, because no strain differences in calcitonin gene-related peptide mRNA content were detected in heart or brain.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

In vivo 31P nuclear magnetic resonance measurements in canine heart using a catheter-coil.

We have developed a new method of obtaining high resolution 31P nuclear magnetic resonance spectra from canine heart without the need for major surgery. This is done by passing an elliptical nuclear magnetic resonance receiver coil through a peripheral blood vessel into the right or left ventricle. This technique enables spectra to be obtained from a defined region of myocardium in less than 7 minutes (for the right ventricle) with a signal:noise ratio of greater than 9:1. With this catheter-coil, useful cardiac metabolic information will be obtainable, not only from specified regions of the heart, but also from various layers of myocardium.

Animals↗

PubMed1994

Smooth muscle myosin heavy chain exclusively marks the smooth muscle lineage during mouse embryogenesis.

We cloned a portion of the mouse smooth muscle myosin heavy chain (SM-MHC) cDNA and analyzed its mRNA expression in adult tissues, several cell lines, and developing mouse embryos to determine the suitability of the SM-MHC promoter as a tool for identifying smooth muscle-specific transcription factors and to define the spatial and temporal pattern of smooth muscle differentiation during mouse development. RNase protection assays showed SM-MHC mRNA in adult aorta, intestine, lung, stomach, and uterus, with little or no signal in brain, heart, kidney, liver, skeletal muscle, spleen, and testes. From an analysis of 14 different cell lines, including endothelial cells, fibroblasts, and rhabdomyosarcomas, we failed to detect any SM-MHC mRNA; all of the cell lines induced to differentiate also showed no detectable SM-MHC. In situ hybridization of staged mouse embryos first revealed SM-MHC transcripts in the early developing aorta at 10.5 days post coitum (dpc). No hybridization signal was demonstrated beyond the aorta and its arches until 12.5 to 13.5 dpc, when SM-MHC mRNA appeared in smooth muscle cells (SMCs) of the developing gut and lungs as well as peripheral blood vessels. By 17.5 dpc, SM-MHC transcripts had accumulated in esophagus, bladder, and ureters. Except for blood vessels, no SM-MHC transcripts were ever observed in developing brain, heart, or skeletal muscle. These results indicate that smooth muscle myogenesis begins by 10.5 days of embryonic development in the mouse and establish SM-MHC as a highly specific marker for the SMC lineage. The SM-MHC promoter should therefore serve as a useful model for defining the mechanisms that govern SMC transcription during development and disease.

Amino Acid Sequence↗

PubMed1996

Reduced gene expression of vascular endothelial NO synthase and cyclooxygenase-1 in heart failure.

Endothelium-dependent responses are depressed in coronary and peripheral blood vessels after the onset of pacing-induced heart failure in dogs and heart failure of various etiologies in humans. The present study was designed to examine whether these responses were due to decreases in the expression of endothelial cell NO synthase (ecNOS) and cyclooxygenase-1 (COX-1). After 1 month of left ventricular pacing, 8 mongrel dogs were monitored for heart failure as defined by clinical signs and left ventricular end diastolic pressures > 25 mm Hg. Total RNA and protein were isolated from endothelial cells scraped from the thoracic aorta and analyzed by Northern and Western blotting, respectively. Blots probed with 32P-labeled cDNAs for ecNOS and COX-1 were quantified densitometrically, and results were normalized against GAPDH or von Willebrand factor (vWF). In arbitrary units, the ratios of ecNOS to GAPDH were 2.66 +/- 0.77 (mean +/- SEM, n = 17) and 1.12 +/- 0.37 (n = 6 and the ratios of COX-1 to GAPDH were 1.52 +/- 0.52 and 0.56 +/- 0.15 before and after heart failure, respectively. These represent 56% to 64% (P < .05) reductions in ecNOS and COX-1 gene expression. There was no change in the ratios of either COX-1 or ecNOS to vWF. There was also a marked reduction in ecNOS protein after heart failure, estimated at 70%. A marked reduction in nitrite production, a measure of enzyme activity, from thoracic aortas in response to stimulation by either acetylcholine or bradykinin also occurred. To determine whether ecNOS and COX-1 could be independently regulated, an orally active NO-releasing agent, CAS 936, was given to 7 normal dogs for 7 days, and aortic ecNOS and COX-1 mRNAs were analyzed. The ratio of ecNOS to GAPDH was depressed by 52% (P < .05) in aortas from these dogs, whereas the ratio of COX-1 to GAPDH was unchanged. Similar results were found when data were normalized to vWF. These results suggest that at least two endothelial vasodilator gene products are reduced in heart failure, as opposed to a selective defect in NO synthase gene expression.

Animals↗

PubMed2003

Vitamin E reduces transendothelial migration of neutrophils and prevents lung injury in endotoxin-induced airway inflammation.

We investigated the pharmacologic effects of the antioxidant Vitamin E (alpha-tocopherol [alpha-toc]) in airway inflammation induced by inhaled endotoxin. A preparation of alpha-toc incorporated in liposomes was administered intraperitoneally in mice 1 h after exposure of aerosolized endotoxin. Injection of 50 mg alpha-toc/kg significantly decreased the number of neutrophils in airspaces and prevented lung injury, monitored both as decreased lactate dehydrogenase activity in airways and reduced lung edema when compared with animals treated with plain liposomes. Immunofluorescence staining of lung tissue revealed that treatment with alpha-toc decreased the number of neutrophils in lung interstitium, whereas the number in lung blood vessels and peripheral blood did not differ between mice treated with alpha-toc and control mice. Our results indicate that alpha-toc downmodulates the migration of neutrophils across the endothelial barrier, but in contrast to strong anti-inflammatory drugs such as corticosteroids, without inhibition of transcription factors involved in the early inflammatory response (nuclear factor-kappaB/activator protein-1). Neither was the endotoxin-induced expression of proinflammatory cytokines in lung tissue downregulated. Treatment with a combination of alpha-toc and a suboptimal dose of 0.5 mg/kg dexamethasone enhanced the effect, suggesting that alpha-toc, in combination with low doses of corticosteroids, might be effective for therapeutic treatment of acute lung injury.

Animals↗

PubMed1983

The digital circulation in congestive heart failure.

Congestive heart failure (CHF) is a complex clinical entity which is still little understood pathophysiologically. Unless it is in the intractable state it responds well to therapy. It has been known for many years that the peripheral circulation can be dramatically altered when CHF is progressively and rapidly developing and worsening. As compensation develops, these changes gradually return to normal. We have long been studying the digital circulation of patients with CHF and have been impressed with the changes in the behavior of the peripheral blood vessels in these patients.

Air Conditioning↗

PubMed2001

Naratriptan.

Naratriptan is a selective 5-HT(1B/1D) receptor agonist, with a high affinity at the 5-HT(1B), 5-HT(1D) and 5-HT(1F) receptor subtypes. Naratriptan contracts a number of large isolated cerebral arteries from several species, and has little contractile effect on peripheral blood vessels. It has an inhibitory effect on the cranial neurogenic inflammation model. The clinically recommended dose is 2.5 mg. It was found significantly superior to placebo on headache relief and pain free at 2 and 4 hours, and in relieving nausea, photophobia and phonophobia. It also has a good within-patient consistency, and a low recurrence rate. The side-effect profile is that of the triptan class, wih an incidence no different from placebo at the 25 mg dose. The contraindications are similar to any triptan, including coronary disease. Naratriptan is unlikely to affect metabolism of other drugs. In comparison sumatriptan 100 mg, naratriptan 2.5 mg has a slower onset of action and a lower response rate at 4 h, but it has a lower recurrence rate, and is better tolerated.

Humans↗

PubMed1983

Studies on the hypotensive effects of platelet activating factor (PAF, 1-O-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine) in rats, guinea pigs, rabbits, and dogs.

Platelet activating factor (PAF) showed profound and long-lasting hypotensive effects in normotensive and spontaneously hypertensive rats, guinea pigs, rabbits and dogs. Sensitivity to PAF was different among the animal species. The magnitude and duration of the hypotensive effect was dose-dependent. Pharmacological studies suggested that the hypotensive action was unlikely to be caused by the actions on the central or autonomic nervous systems but seemed to be mainly due to some direct action(s) on the peripheral blood vessels.

Animals↗

PubMed1991

Nicorandil (2-nicotinamidoethyl nitrate) inhibits both vaso-dilating and -constricting effects of endothelin in a vascularly isolated hind-limb preparation in rats.

Effects of nicorandil (2-nicotinamidoethyl nitrate), a nitrate derivative with a K+ channel-opening action, on endothelin-1 (ET)-induced effects on peripheral blood vessels were studied using a hind-limb perfusion preparation in rats. ET injected into this circuit increased the perfusion pressure for more than 30 min following a transient, initial vasodepression of the perfusion system. The magnitude of both responses was dose-dependent. Pretreatments with nicorandil infused into this preparation significantly attenuated both the initial vasodilation and the sustained vasoconstriction caused by ET. The initial vasodepression caused by ET could be mediated by the release of endothelium-derived relaxing factor (EDRF). The sustained phase would be due to increased intracellular calcium elicited by ET. Nicorandil inhibited both the initial and the sustained phase of the ET-responses, probably by inhibition of intracellular phosphoinositide metabolism in both endothelium and vascular smooth muscle cells.

Analysis of Variance↗

PubMed1979

Action of depressor-I, a hypotensive phospholipid from bovine brain, on systemic and arterial blood pressures of various species.

Effects of "Depressor-I" (D-I), a new hypotensive phospholipid obtained from bovine brain lipid fraction, on systemic arterial blood pressure were investigated. The hypotensive activity of D-I in urethane anaesthetized rats was dose dependent and tachyphylaxis and/or sensitization were not observed. Increments of the respiration and the heart rate were observed with sharp falls in blood pressures following intravenous administration of D-I, in simultaneous recordings in anaesthetized rats. D-I elicited hypotension in all species of animals examined, and the sensitivities to D-I were much the same, however, there were two types in patterns of duration on responses and the durations were also dose dependent. D-I exhibited depressor-responses even in conscious rats, though responses were much smaller compared with those seen in anaesthetized rats. In a comparison of anaesthetic agents in rats, the highest hypotensive activity of D-I was observed with pentobarbital anaesthesia, a moderate response was seen with alpha-chloralose and the least response was seen with urethane. In spinal rats or those pretreated with reserpine or antagonists, such as atropine, diphenhydramine, propranolol and hexamethonium, D-I also elicited hypotension. These results suggest that "Depressor-I" does not elicit the depressor action via the stimulation of the central and the autonomic nervous systems but rather by a direct action on peripheral blood vessels.

Anesthesia↗

PubMed1981

Effects of guanabenz on the adrenergic mechanism in rabbit arterial strips.

Effects of guanabenz, a hypotensive agent, on the adrenergic mechanism were studied in isolated rabbit thoracic aorta and pulmonary artery and findings were compared with data obtained with clonidine and guanethidine. Guanabenz in concentrations higher than 10(-6) M produced weak contractions which were attenuated by phentolamine or yohimbine. Such concentrations of guanabenz competitively inhibited the contractile response to noradrenaline, but did not attenuate the response to tyramine. In concentrations ranging from 10(-8) to 10(-7) M, guanabenz attenuated the contraction and the increase of 3H-efflux in response to transmural electrical stimulation of the pulmonary artery preincubated with 3H-noradrenaline. Phentolamine or yohimbine effectively blocked these inhibitory effects of guanabenz. Such effects of guanabenz were similar to those of clonidine and dissimilar to those of guanethidine. These results indicate that guanabenz acts on presynaptic and postsynaptic alpha receptors of the peripheral blood vessels, as in the case of clonidine and that the potency was almost the same as clonidine.

Animals↗

PubMed1982

Reversible hypertension caused by calcium overloading in a patient with postoperative hypoparathyroidism.

A 37-year-old woman with postoperative hypoparathyroidism had hypertension, and elevated plasma renin activity (PRA) and subsequent hyperaldosteronism during a two-month hypercalcemic period caused by vitamin D and excessive calcium supplements. The hypertension with elevated PRA, however, was resistant to the angiotensin II (AII) analog [Sar1, Ile8] ALL. PRA further increased and plasma aldosterone decreased in response to the [Sar1, Ile8] ALL. When the patient became normocalcemic, normotensive and normoreninemic, calcium gluconate (5 mg calcium/kg/h) was infused for one hour. The calcium infusion reproduced hypercalcemic hypertension mediated by an increase in total peripheral resistance. These observations suggest that the hypertension observed while taking vitamin D and excessive calcium supplements may be caused by a direct effect of calcium on peripheral blood vessels and the renin-angiotensin system may play a negligible role.

Adult↗