scholarly journals Sexual Dimorphism of Cardiovascular Ischemia Susceptibility Is Mediated by Heme Oxygenase

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Anikó Pósa ◽  
Krisztina Kupai ◽  
Rudolf Ménesi ◽  
Zita Szalai ◽  
Renáta Szabó ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sexual Dimorphism ◽  
Heme Oxygenase ◽  
Blood Pressure Response ◽  
Isolated Heart ◽  
Reproductive Age ◽  
Female Rat ◽  
Heart Perfusion ◽  
Basal Blood Pressure

We investigated the gender differences in heme-oxygenase (HO) enzyme, which produces endogenous vascular protective carbon monoxide (CO). We studied (1) the activity and expression of HO enzymes in the left ventricle (LV) and aorta, (2) basal increase in basal blood pressure provoked by arginine vasopressine (AVP)in vivo, (3) the heart perfusion induced by AVP, (4) the ST segment depression provoked by adrenaline and 30 seconds later phentolamine, and (5) the aorta ring contraction induced by AVP in female and male Wistar rats. We found that HO activity and the expression of HO-1 and HO-2 were increased in female rat aorta and LV. We demonstrated that the basal blood pressure and administration of AVP provoked blood pressure response are increased in the males; the female myocardium was less sensitive towards angina. Both differences could be aggravated by the inhibition of HO. The aorta rings were more susceptible towards vasoconstriction by AVP in males; isolated heart perfusion decrease was higher in males. The HO inhibition aggravated the heart perfusion in both sexes. In conclusion, the increased HO activity and expression in females might play a role in the sexual dimorphism of cardiovascular ischemia susceptibility during the reproductive age.

scholarly journals Cardioprotective Effect of Selective Estrogen Receptor Modulator Raloxifene Are Mediated by Heme Oxygenase in Estrogen-Deficient Rat

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Anikó Posa ◽  
Renáta Szabó ◽  
Krisztina Kupai ◽  
Anikó Magyariné Berkó ◽  
Médea Veszelka ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heme Oxygenase ◽  
Blood Pressure Response ◽  
Pharmacological Inhibition ◽  
Beneficial Effects ◽  
Receptor Modulator ◽  
St Segment ◽  
Inflammatory State ◽  
Negative Impacts

Estrogens and raloxifene (RAL) have beneficial effects on certain cardiovascular indices in postmenopausal women characterized by estrogen deficiency. Heme oxygenase (HO) activity is increased by 17β-estradiol (E2) and RAL in estrogen-deficient rat resulting in vasorelaxation mediated by carbon monoxide. We determined the expressions of HO in cardiac and aortic tissues after ovariectomy (OVX) and subsequent RAL or E2treatment. We investigated the effects of pharmacological inhibition of HO enzyme on the arginine vasopressin- (AVP-) induced blood pressure in vivo, the epinephrine- and phentolamine-induced electrocardiogram ST segment changes in vivo, and the myeloperoxidase (MPO) enzyme activity. When compared with intact females, OVX decreased the HO-1 and HO-2 expression, aggravated the electrocardiogram signs of heart ischemia and the blood pressure response to AVP, and increased the cardiac MPO. E2and RAL are largely protected against these negative impacts induced by OVX. The pharmacological inhibition of HO in E2- or RAL-treated OVX animals, however, restored the cardiovascular status close to that observed in nontreated OVX animals. The decreased expression of HO enzymes and the changes in blood pressure ischemia susceptibility and inflammatory state in OVX rat can be reverted by the administration of E2or RAL partly through its antioxidant and anti-inflammatory roles.

Maintenance of endothelial function following acute resistance exercise in females is associated with a tempered blood pressure response

2020 ◽  
Vol 129 (4) ◽  
pp. 792-799 ◽  
Author(s):  
Takuma Morishima ◽  
Jaume Padilla ◽  
Yosuke Tsuchiya ◽  
Eisuke Ochi
Keyword(s):  
Blood Pressure ◽  
Sexual Dimorphism ◽  
Endothelial Function ◽  
Resistance Exercise ◽  
Blood Pressure Response ◽  
Pressure Response ◽  
Healthy Male ◽  
Vascular Effects ◽  
First Time ◽  
Female Subjects

The present data demonstrate for the first time that acute resistance exercise impairs endothelial function in young, healthy male but not female subjects. In addition, we show that the preservation of endothelial function in females is associated with a mitigated blood pressure response during resistance exercise. Accordingly, this work portrays a sexual dimorphism in the barostress response, and ensuing vascular effects, to resistance exercise.

scholarly journals Human neuropeptide Y potentiates α1-adrenergic blood pressure responses in vivo

1998 ◽  
Vol 275 (3) ◽  
pp. H760-H766 ◽  
Author(s):  
Leander V. Schuerch ◽  
Lilly M. Linder ◽  
Eric Grouzmann ◽  
Walter E. Haefeli
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Neuropeptide Y ◽  
Blood Pressure Response ◽  
Human Hand ◽  
Response Curves ◽  
Fourfold Increase ◽  
Dose Rates ◽  
Blood Pressure Responses

Human neuropeptide Y (hNPY) potentiates the postjunctional vasoconstrictor effects of α1-adrenoceptor agonists in animals and in human hand veins in vivo. We therefore hypothesized that such an interaction might also occur in the human arterial bed. With the present single-blind cross-over study in 12 healthy volunteers, the effect of subpressor doses of hNPY on the blood pressure response to α1-adrenoceptor stimulation was evaluated. Dose-response curves were constructed to intravenously infuse phenylephrine with and without coinfusion with two different doses of hNPY (1.4 and 14.3 pmol ⋅ kg−1 ⋅ min−1). Blood pressure, heart rate, and forearm blood flow were recorded, and plasma hNPY was determined. During infusion of the higher hNPY dose, which increased hNPY from 24.0 ± 12.0 to 495.1 ± 12.6 pmol/l, blood pressure curves were 2.4-fold shifted toward lower phenylephrine dose rates ( P < 0.001). Forearm vascular resistance showed a similar trend, whereas the counterregulatory decrease of heart rate was similar in both groups. In contrast, the lower hNPY dose rate producing a fourfold increase in hNPY concentrations did not modify the response to phenylephrine. This in vivo study in humans demonstrates that hNPY induced potentiating effects on α1-adrenergic constriction also in the systemic arterial circulation and suggests that circulating hNPY may participate in the control of vascular tone.

scholarly journals Cardioprotective Effects of Voluntary Exercise in a Rat Model: Role of Matrix Metalloproteinase-2

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Anikó Pósa ◽  
Renáta Szabó ◽  
Krisztina Kupai ◽  
Zoltán Baráth ◽  
Zita Szalai ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Infarct Size ◽  
Voluntary Exercise ◽  
Matrix Metalloproteinase 2 ◽  
Moderate Intensity ◽  
Protective Mechanism ◽  
Ring Contraction ◽  
Aorta Ring ◽  
Heart Perfusion ◽  
Basal Blood Pressure

Background. Regular exercise at moderate intensity reduces cardiovascular risks. Matrix metalloproteinases (MMPs) play a major role in cardiac remodeling, facilitating physiological adaptation to exercise. The aim of this study was to examine the influence of voluntary physical exercise on the MMP-2 enzyme activity and to investigate the cardiac performance by measurement of angina susceptibility of the heart, the basal blood pressure, the surviving aorta ring contraction, and the cardiac infarct size after I/R-induced injury.Methods. Male Wistar rats were divided into control and exercising groups. After a 6-week period, the serum level of MMP-2, basal blood pressure, cardiac angina susceptibility (the ST segment depression provoked by epinephrine and 30 s later phentolamine), AVP-induced heart perfusion and aorta ring contraction, infarct size following 30 min ischemia and 120 min reperfusion, and coronary effluent MMP-2 activity were measured.Results. Voluntary wheel-running exercise decreased both the sera (64 kDa and 72 kDa) and the coronary effluent (64 kDa) MMP-2 level, reduced the development of ST depression, improved the isolated heart perfusion, and decreased the ratio of infarct size.Conclusion. 6 weeks of voluntary exercise training preserved the heart against cardiac injury. This protective mechanism might be associated with the decreased activity of MMP-2.

scholarly journals Inhibition of NOX1 mitigates blood pressure increases in elastin insufficiency

Function ◽  
2021 ◽  
Author(s):  
Angela Troia ◽  
Russell H Knutsen ◽  
Carmen M Halabi ◽  
Daniela Malide ◽  
Zu Xi Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Reactive Oxygen Species ◽  
Systolic Blood Pressure ◽  
Blood Pressure Response ◽  
Reactive Oxygen ◽  
Vascular Wall ◽  
Vascular Stiffness ◽  
Oxygen Species

Abstract Elastin insufficiency leads to the cardiovascular hallmarks of the contiguous gene deletion disorder, Williams-Beuren syndrome, including hypertension and vascular stiffness. Previous studies showed that Williams-Beuren syndrome deletions that extended to include the NCF1 gene were associated with lower blood pressure and reduced vascular stiffness. NCF1 encodes for p47phox, the regulatory component of the NOX1 NADPH oxidase complex, that generates reactive oxygen species in the vascular wall. Dihydroethidium and 8-hydroxyguanosine staining of mouse aortas confirmed that Eln heterozygotes (Eln+/-) had greater reactive oxygen species (ROS) levels than wild types (Eln+/+), a finding that was negated in vessels cultured without hemodynamic stressors. To analyze the Nox effect on elastin insufficiency, we utilized both genetic and chemical manipulations. Both Ncf1 haploinsufficiency (Ncf1+/-) and Nox1 insufficiency (Nox1-/y) decreased oxidative stress and systolic blood pressure in Eln+/- without modifying vascular structure. Chronic treatment with apocynin, a p47phox inhibitor, lowered systolic blood pressure in Eln+/-, but had no impact on Eln+/+ controls. In vivo dosing with phenylephrine produced an augmented blood pressure response in Eln+/- relative to Eln+/+, and genetic modifications or drug-based interventions that lower Nox1 expression reduce the hypercontractile response to phenylephrine in Eln+/- mice to Eln+/+ levels. These results indicate that the mechanical and structural differences caused by elastin insufficiency leading to oscillatory flow can perpetuate oxidative stress conditions which are linked to hypertension, and that by lowering the Nox1-mediated capacity for vascular ROS production, blood pressure differences can be normalized.

Comparative Pharmacology of New Specific Angiotensin Antagonists

1974 ◽  
Vol 48 (s2) ◽  
pp. 19s-21s
Author(s):  
B. A. Schoelkens
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Blood Pressure Response ◽  
Renal Hypertension ◽  
Antagonistic Activity ◽  
Conscious Rats ◽  
Blood Pressures ◽  
Colon Ascendens

1. The angiotensin II antagonism by newly synthesized 8-C-phenylglycine analogues of [5-isoleucine]angiotensin II in different preparations was investigated in vitro and in vivo. 2. All analogues competitively inhibited the myotropic effect of angiotensin II on the isolated colon ascendens of the guinea-pig and the stomach of the rat. 3. In normotensive dogs, cats, rabbits, guinea-pigs and rats the blood pressure response to infused angiotensin II was inhibited by the antagonists. The angiotensin II-induced fall in renal blood flow in the dog was blocked during infusion of the analogues. Acute renal hypertension in rats was significantly decreased. Of conscious rats variously with normal blood pressures, spontaneous hypertension and chronic renal hypertension, only in the last group could a marked uniform fall in blood pressure be demonstrated. The central pressor effect of angiotensin II was also inhibited in conscious rats. 4. 8-C-Phenylglycine analogues of [5-isoleucine]-angiotensin II exhibit a specific antagonistic activity to endogenous and exogenous angiotensin II.

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