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At least 19 recordsLinked to original sources
PubMed1991

Effects of dietary calcium on blood pressure, vascular reactivity and vascular smooth muscle calcium efflux rate in Zucker rats.

Previous data from this laboratory indicate that hypertension in insulin resistant Zucker obese rats is accompanied by an impairment in vascular smooth muscle Ca2+ efflux. Since insulin resistant states are also generally salt-sensitive and dietary Ca2+ reduces blood pressure in some salt-sensitive states, we evaluated the effects of dietary Ca2+ on blood pressure and vascular reactivity and examined whether these effects are due to increased vascular smooth muscle Ca2+ efflux. We assigned 16 obese and 16 lean rats to a normal (0.5%) or high (1.5%) Ca2+ diet for 28 days, following which intraarterial blood pressure and in vitro vascular smooth muscle 45Ca efflux and vascular reactivity responses to phenylephrine and serotonin were measured. Blood pressure was elevated in the obese rats on both diets (P less than 0.2), and the high calcium diet lowered both systolic and diastolic pressure in both the lean and obese rats (P less than 0.5). Vascular reactivity was higher in the obese rats (P less than 0.2), but dietary Ca2+ exerted opposite effects on vascular reactivity to the agonists. High Ca2+ reduced sensitivity to serotonin in the obese rats by 54% (P less than .05) without affecting sensitivity in the lean rats. In contrast, the high Ca2+ diet increased sensitivity to phenylephrine by 31% in both groups (P less than .01). 45Ca efflux was lower in the obese rats compared to the lean rats (P less than .05), and the high Ca2+ diet increased this rate by 23% in the lean, but not the obese, rats (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1977

Vascular reactivity of perfused vascular bed in spontaneously hypertensive and normotensive rats.

1 Hypertensive and normotensive rats of the same age group were isolated from an inbred colony of spontaneously hypertensive rats. 2 The perfused hindquarter and mesenteric artery preparations obtained from hypertensive and normotensive rats exhibited an increased reactivity to noradrenaline (NA) and angiotensin II. 3 Dose-response curves to NA obtained from hypertensive and normotensive rats exhibited a steeper slope and higher maximum than those from control rats. 4 These findings suggest that increased vascular reactivity of blood vessels is independent of the development or maintenance of elevated blood pressure.

Angiotensin II↗
PubMed1995

Vascular reactivity: a measurement of calcium channel blockade.

Clinical studies have shown that calcium antagonist drugs interfere with the reactivity of vascular smooth muscle and thereby attenuate the pressor responses to adrenergic and non-adrenergic vasoconstrictor agents. It is, therefore, possible to explore the extent and duration of calcium channel blockade by studying the magnitude and time course of the attenuation of pressor responses. The effects of three long-acting calcium antagonists, amlodipine, lacidipine and nifedipine GITS (gastrointestinal therapeutic system), on vascular reactivity were assessed over 24h and 48h dosage intervals. It was shown that all three agents attenuate the vasoconstrictor responses to both adrenergic and non-adrenergic stimuli. However, amlodipine and nifedipine GITS were found to suppress vascular reactivity more consistently than lacidipine over 24h. Extending the analysis to 48h after dosing showed that amlodipine had the most consistent effect.

Amlodipine↗
PubMed1986

Hydralazine inhibits vascular reactivity by a mechanism independent of vascular prostaglandin biosynthesis: role of thromboxane synthetase in blocking hydralazine actions.

To explore the mechanism of action of hydralazine on vascular reactivity of small vessels we have examined its actions in the isolated perfused mesenteric vascular bed. In buffer perfused preparations hydralazine inhibited responses to nondepolarizing stimuli at concentrations comparable to those achieved in vivo. Inhibition of cyclo-oxygenase activity enhanced hydralazine's action as did inhibition of thromboxane synthetase. Hydralazine stimulated mesenteric vascular bed prostaglandin biosynthesis (6-keto PGF1a and PGE2 determined by radio-immunoassay) and stimulated aorta PG12 synthesis (monitored by platelet bioassay). Extracellular calcium opposed hydralazine's action by a mechanism sensitive to cyclo-oxygenase inhibition. Concentrations of hydralazine substantially greater than those effective in the perfused vascular bed were required to demonstrate inhibition of platelet aggregation and ram seminal vesicles cyclooxygenase activity. These data indicate: Hydralazine acts directly on the smooth muscle to attentuate responses to nondepolarizing stimuli. Hydralazine does not inhibit vascular reactivity by a PG12 dependent mechanism although it stimulates prostaglandin biosynthesis. Reduction of vascular bed prostaglandin and thromboxane A2 biosynthesis enhances hydralazine actions. Hydralazine appears to act at a thromboxane A2 sensitive site however it is not a nonselective prostaglandin antagonist. Hydralazine is effective at concentrations which do not inhibit either platelet aggregation or ram seminal vesicle cyclooxygenase. These data suggest that hydralazine is a potent direct acting vasodilator which stimulates prostaglandin biosynthesis and whose potency may in turn be attenuated by the production of proconstrictory prostaglandins.

Animals↗
PubMed1988

[The interrelation of the sodium-excretory function of the kidneys and vascular reactivity in hypertension patients].

Vascular reactivity was evaluated by a modified photoplethysmographic method in 20 patients with essential hypertension before and after an acute volumetric salt load. A relationship was demonstrated between vascular reactivity and renal sodium excretion pattern under stress. Patients with "excessive" natriuresis 24 h after the test showed reduced vascular reactivity, and slow sodium and water excretion was associated with increased vascular response. A study of membrane Ca2+ transport 24 h after the test showed an increase in receptor-dependent Ca2+ uptake in response to all inductors (platelet aggregation factor, vasopressin, ADP), as compared to the baseline.

Adult↗
PubMed2006

Short-term and long-term FK506 treatment alters the vascular reactivity of renal and mesenteric vascular beds.

The aims of this study were to investigate the role of endothelin-1 in FK506-induced hypertension and vascular dysfunction of rats treated with the drug for 8 (short-term) or 30 (long-term) days and to measure malondialdehyde levels in the kidneys. Kidney and mesentery of rats were perfused. In the short-term treated groups, there was no significant change in systolic blood pressure. The response to noradrenaline only in renal vascular beds was significantly increased by FK506 and this increase was prevented by Bosentan. FK506 had no significant effect on sodium nitroprusside-induced vasodilation in comparison with solvent in both vascular beds. Bosentan failed to prevent these responses. In the long-term treated groups, at the end of the treatment with FK506, there was a significant increase in blood pressure, but no change in the response to noradrenaline in either kidneys or mesentery. The increase in blood pressure was prevented by bosentan treatment. FK506 increased malondialdehyde levels in the kidneys of the rats from only the long-term treated groups. Bosentan did not change this increase. Our results indicated that endothelin-1 plays a key role in the FK506-induced change in vascular reactivity to noradrenaline in renal vascular beds and drug-induced hypertension in the rats. There was no relationship between oxidative stress and FK506-induced hypertension.

Animals↗
PubMedDate not supplied

Inhibition of Ras-GTPase improves diabetes-induced abnormal vascular reactivity in the rat perfused mesenteric vascular bed.

OBJECTIVE: The signalling mechanisms involved in regulating altered vascular reactivity in diabetes are not fully understood. The aim of this study was to investigate the role of Ras-GTPase in the development of abnormal vascular reactivity in diabetes. MATERIALS AND METHODS: We investigated the ability of chronic administration of FPTIII (1.5 mg/kg), an inhibitor of Ras-GTPase, to modulate the altered vasoreactivity of the rat perfused mesenteric bed to common vasoconstrictors and vasodilators in streptozotocin (STZ)-induced diabetes. RESULTS: The vasoconstrictor responses induced by norepinephrine (NE) and endothelin-1 (ET-1) were significantly increased whereas vasodilator responses to carbachol, histamine and isoprenaline were significantly reduced in the perfused mesenteric bed of the STZ-diabetic rats. Inhibition of Ras-GTPase by chronic administration of FPTIII produced a significant normalization of the altered agonist-induced vasoconstrictor and vasodilator responses without affecting blood glucose levels. Inhibition of Ras-GTPase did not affect the agonist-induced vasoconstrictor and vasodilator responses in the control animals. CONCLUSION: These data suggest that signal transduction pathways activated by Ras-GTPase are involved in the development of diabetic vascular dysfunction. Potential strategies aimed at modifying actions of signal transduction pathways involving Ras-GTPase may therefore prove to be beneficial in treatment of vascular complications in diabetes.

Animals↗
PubMed1980

Pregnancy blunts pulmonary vascular reactivity in dogs.

Pregnancy decreases systemic vascular reactivity but comparatively little is known about the effects of pregnancy on the pulmonary circulation. Pulmonary vascular resistance (PVR) during acute hypoxia was lower (P < 0.01) in eight intact anesthetized pregnant dogs compared to the same animals postpartum. Mean pulmonary arterial pressure (Ppa) and PVR during infusion of prostaglandin (PG) F2 alpha were also reduced during pregnancy. Nonpregnant female dogs (n = 5) treated with estrogen (0.001 mg x kg-1 x da-1) for 2 wk had decreased Ppa (P < 0.01) during acute hypoxia compared to control measurements, but PVR was unchanged during hypoxia and PGF2 alpha infusion. Treatment with progesterone in four dogs had no effect on pulmonary vascular reactivity to hypoxia or PGF2 alpha. Inhibition of circulating PG with meclofenamate in four dogs during pregnancy did not appear to restore pulmonary vascular reactivity. Blunted pulmonary vascular reactivity is suggested by the limited data available for women, but is not seen in pregnant cows. We conclude that pregnancy decreases pulmonary as well as systemic vascular reactivity in the dog, but the mechanism is unclear.

Animals↗
PubMed1994

The influence of different amounts of n-3 polyunsaturated fatty acids on bleeding time and in vivo vascular reactivity.

Mesenteric bleeding time, mesenteric vascular reactivity, platelet and erythrocyte lipid fatty acid composition were measured at 2-3 weeks, 5-6 weeks and 11-22 weeks in normotensive Wistar rats, fed on high (6.5% energy) or moderate (1.6% energy) intakes of eicosapentaenoic acid (20:5n-3; EPA) as fish oil, compared with controls fed on a diet devoid of EPA. All diets contained the same level of linoleic acid (4% energy): the moderate- and high-EPA diets also contained 1.1 and 4.4% of the energy as docosahexaenoic acid (22:6n-3) respectively. Moderate, but not high, intakes of EPA increased mesenteric bleeding time. Similar reductions in erythrocyte and platelet arachidonic acid (20:4n-6) occurred in animals fed on either high or low amounts of EPA, but the proportion of EPA increased dose-dependently. At high intakes of EPA the proportion of oleic acid in platelets and erythrocytes was decreased. Blood pressure platelet counts, mesenteric vessel diameter and mesenteric vascular reactivity to vasopressin were unaffected by treatment. High intakes of fish oil led to a slight fall in packed cell volume. In a second experiment bleeding time and mesenteric vascular reactivity to noradrenaline were increased 2-4 weeks after receiving a moderate intake of EPA and these effects persisted 5-21 d after switching to a control diet. A similar increase in vascular reactivity to noradrenaline was observed in animals given indomethacin (6 mg/kg) but not in those given aspirin (20 mg/kg).

Animals↗
PubMedDate not supplied

Adverse effects of reactive oxygen species on vascular reactivity in insulin resistance.

Insulin resistance (IR) has adverse effects on the reactivity of arteries and arterioles and promotes arterial hypertension and vascular occlusive diseases. Altered reactivity of resistance vessels occurs at both the endothelium and smooth-muscle levels. One major mechanism of vascular dysfunction with IR involves the augmented generation, availability, and/or actions of reactive oxygen species (ROS). Scavengers of ROS are able immediately to restore normal dilator responsiveness in arteries from IR animals. Other factors, such as increased importance of constrictor agents such as endothelin, also restrict normal dilator responses. The basis of ROS-mediated vascular dysfunction in IR may be secondary to underlying inflammatory processes throughout the arterial wall. Although ROS scavengers may be beneficial in the short term, prolonged treatments involving behavioral approaches, such as changes in diet, weight loss, and regular exercise, and pharmacological approaches, involving the use of insulin-sensitizing agents, inhibitors of the renin-angiotensin system, or administration of statins, appear to offer benefits against the detrimental vascular effects of IR. Nonetheless, the most effective approach appears to involve prevention of IR via adoption of a healthy lifestyle by young people.

Acetylcholine↗
PubMed1984

[Digital dynamic telethermography: an aid in the study of vascular reactivity to cold].

Vascular reactivity to cold has been studied on 22 patients by means of digital dynamic thermography. Using an interface the thermographic images are digitized in real time and stocked in the computer. After the cooling (two minutes in water at 10 degrees C) the warming-up is followed by sequential thermographic images. Profiles of thermic evolution are represented for 12 regions of interest (at the level of each finger and two for the back of the hands). Four types of thermic profiles are observed: Type 0: all fingers and back of hands have the same basal temperature. After cooling the warming-up is immediate, synchronic for all fingers and goes on more or less rapidly. Type I: at the basal state all fingers have identical temperature. After cooling, the warming-up starts after a latency period of several minutes, which is identical for all fingers. After it the warming-up is fast and synchronic with a thermic "overshot" phenomenon at the end of the examination. Only the thumbs are warmed-up without a latency period. Type II: a latency period similar that of type I is observed but the following warming-up takes place with variable speeds for each considered finger. Type III: at the basal state the fingers are colder than the back of the hand. Spontaneously, some fingers are warmed only by the influence of the hand vertical position. After cooling, the warming-up takes place with variable speeds and after variable latency periods which are a characteristic of each finger.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Vessels↗
PubMed1995

Collateral development and angiogenesis after major artery ligation does not alter hindquarter vascular reactivity in conscious rabbits.

We tested whether vasodilator and vasoconstrictor responses of the hindquarter vasculature in conscious rabbits were altered 1 day, 2 weeks, and 6 months after bilateral superficial femoral artery ligation (SFAL). With pharmacological autonomic blockade, hindquarter flow (Doppler flowmeter) was restored to 84% of control values 1 day postligation (n = 5). Responses to aortic balloon inflation (5-80 s), and intraaortic infusion of norepinephrine, angiotensin II, serotonin, acetylcholine, sodium nitroprusside, and adenosine were similar to pre-SFAL responses. Two weeks post-SFAL, acrylic casts showed an extensive collateral network originating from branches of internal iliac and deep femoral arteries. Acetylcholine-induced dilatation was attenuated postligation (n = 7) relative to controls (n = 13). Serotonin caused constriction in two rabbits postligation but dilatation in all others; however responses to all other agents tested were similar to controls. Reactive hyperemia and vascular reactivity were similar in rabbits 6 months post-SFAL (n = 5) and controls (n = 5). Thus, despite extensive vascular remodeling after SFAL, global hyperemic flow responses of the rabbit hindquarter vasculature appeared normal. We found only minimal changes in vascular reactivity to constrictor and dilator stimuli. This model of peripheral vascular disease does not reflect the clinical syndrome.

Acetylcholine↗
PubMed1994

Alterations of ex vivo vascular reactivity in intraperitoneal sepsis.

We examined vascular reactivity to vasoconstrictors [phenylephrine (PE), serotonin (5-HT), and high K+] and vasodilators [acetylcholine (ACh), A23187, L-arginine, and nitroglycerin (NTG)] in isolated mesenteric arterial rings from control and septic rats. Sepsis was induced by cecal ligation and puncture (CLP). A possible mechanism underlying CLP-induced alteration in vascular reactivity was also investigated with N omega-nitro-L-arginine (L-NNA 50 microM), methylene blue (MB 10 microM), and indomethacin (5 microM). In vivo, septic rats manifested two distinct hemodynamic phases, a hyperdynamic state during early (9 h after CLP) phase, followed by a hypodynamic state during late (18 h after CLP) phase. Therefore, we examined ex vivo vascular reactivity in these two phases. Results demonstrated that CLP operation caused hyporesponsiveness to contractile agents and hyperresponsiveness to vasodilator agents. After endothelium removal, most of the contractile responses were enhanced in both CLP-operated (9 and 18 h after operation) and sham-operated rats, whereas enhancement of high-K(+)-induced contraction was observed only in denuded rings from CLP 18-h rats. In addition, augmentation of relaxation induced by ACh at 9 or 18 h after CLP was abolished by N omega-nitro-L-arginine or MB but not by indomethacin. A possible mechanism responsible for alterations of vascular reactivity may be overproduction of nitric oxide (NO) which is blocked by L-NNA or MB.

Animals↗
PubMed1985

Vascular reactivity in experimental acute renal failure.

Vascular reactivity in-vivo and in-vitro was examined in rats with acute renal failure produced by bilateral nephrectomy or intramuscular glycerol injection. Bilaterally nephrectomized rats displayed enhanced pressor responses to noradrenaline and angiotensin. However, the contractile responses to noradrenaline, angiotensin and potassium chloride of aortic rings and portal vein segments from nephrectomized rats were not significantly different from the responses obtained in vessels from sham-operated controls. Rats with glycerol-induced ARF which were pretreated with indomethacin had significantly lower pressor responses to noradrenaline and angiotensin than similarly treated control animals. Aortic rings from glycerol-injected rats produced significantly smaller contractions to noradrenaline than preparations from controls. This difference was not abolished by incubation of vessels with indomethacin. The findings suggest that the absence of kidneys or the presence of damaged renal tissue and not uraemia itself have pronounced but opposite effects on vascular reactivity. The depression of vascular reactivity in glycerol-induced ARF does not appear to be a result of increased production of prostaglandins.

Acute Kidney Injury↗
PubMedDate not supplied

Dietary calcium on vascular reactivity in normotensive and spontaneously hypertensive rats.

Vascular reactivity and systolic blood pressure (SBP) were studied in tail artery rings isolated from stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive, Wistar-Kyoto rats (WKY). After a control week on a diet with 1% of calcium, the animals were randomly assigned to three groups, which were fed with 1% (control), 0.4% (low) or 2.5% (high) dietary calcium. Both vascular reactivity and SBP were studied in the same animal during 9 weeks after changing diets. In the SHRSP rats on high Ca diet, maximal contractile responses to norepinephrine and serotonin (10(-10) to 10(-4) M) and to KCl (5 to 105 mM) were markedly decreased at the end of the study with respect to the control diet. These vascular changes were accompanied by a decrease of SBP in the same animals. Low calcium diet prevented the age-related increase of SBP in SHRSP rats and produced vascular changes of a lesser magnitude. WKY rats showed no significant modifications of SBP or vascular reactivity. Since plasmatic Ca2+ levels were not altered, the changes detected could not be attributed to a direct depressant effect of high calcium on the vascular smooth muscle cell (i.e. a "stabilizing action" of calcium). It is speculated that high dietary calcium could modulate the synthesis of calcium binding proteins of the plasma membrane, decreasing vascular reactivity and the elevated vascular resistance which is usually present in hypertension.

Animals↗
PubMed2004

Altered vascular reactivity and KATP channel currents in vascular smooth muscle cells from deoxycorticosterone acetate (DOCA)-salt hypertensive rats.

This study was designed to evaluate the contribution of ATP-dependent potassium (KATP) channels to the changes in vascular reactivity and spontaneous tone observed in vessels isolated from deoxycorticosterone acetate (DOCA)-salt hypertensive rats. In phenylephrine preconstricted aortic rings, cromakalim induced concentration-dependent, glibenclamide-sensitive relaxation. The concentration response curve to cromakalim was shifted to the right in DOCA-salt hypertensive rats (EC50: 0.850 +/- 0.100 microM) compared with SHAM-normotensive rats (0.108 +/- 0.005 microM), and the maximum relaxation (Emax) evoked by cromakalim was significantly lower in aortic rings from the DOCA group (68 +/- 2%) compared with the SHAM group (108 +/- 5%). The results were similar in endothelium-denuded rings. Spontaneous tone was observed in aortic rings (5 g preload) from DOCA-salt but not SHAM rats. Cromakalim abolished spontaneous tone and the effect was blocked by glibencamide. In whole cell patch clamp studies, increasing extracellular K concentrations from 5.4 to 140 mM and the administration of cromakalim evoked dramatic increases in KATP channel currents in aortic cells isolated from SHAM rats. In contrast, in aortic cells from DOCA-salt hypertensive rats, KATP channel currents were either absent or weak in response to challenges by elevated extracellular K and by cromakalim. These findings suggest that the function of KATP channels is impaired in smooth muscle cells from aorta of DOCA-salt hypertensive rats, which may contribute to the impaired vasodilatation and spontaneous tone observed in these rats.

Adenosine Triphosphate↗
PubMed1988

Impaired vascular reactivity during the first two years of diabetes mellitus after initial restoration.

Vascular reactivity was studied prospectively in 36 consecutive children (15 males, 21 females) below 15 years from the county of Uppsala with newly acquired type I diabetes mellitus (IDDM). Skin postocclusive hyperaemia was recorded with a transcutaneous oxygen electrode at 37 degrees C on admission before receiving insulin treatment and 1, 6, 12 and 24 months after diagnosis. Fifty-eight healthy children (25 males, 33 females), served as a reference group. The relations between vascular reactivity and age, sex and a number of biochemical variables that are often disturbed in IDDM were analyzed. On admission, the vascular reactivity was significantly lower in diabetic children than in controls (p less than 0.001). This reduction was normalized during the first month of treatment. After two years of diabetes, the vascular reactivity was again significantly lower in diabetic children than in the control group (p less than 0.001). There was no significant correlation between the vascular reactivity, the lag phase or baseline variables and any of the factors mentioned above at any time of investigation, except that serum magnesium was significantly correlated with vascular reactivity after six months of IDDM. It is suggested that the mechanism underlying an impairment of vascular reactivity on admission (reversible) is different from that of the late reduction, which might be a very early manifestation of the later structural diabetic microangiopathy.

Adolescent↗