scholarly journals ANTAGONISM IN SYSTEM REGULATION ARTERIAL PRESSURE And ITS CHANGE after THERAPY NICERGOLINE

2021 ◽  
Vol 4 (11(75)) ◽  
pp. 58-67
Author(s):  
A. Shutov ◽  
A. Matskanjuk
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Peripheral Vascular Resistance ◽  
Hierarchical Level ◽  
Peripheral Vascular ◽  
Dynamic Series

By the method of fractional trends, when analyzing the dynamic series of blood pressure (АД), an antagonism between the cardiac output block (CB) and the peripheral vascular resistance block (СПС) was revealed in the patient, after 12 weeks of nicergoline therapy, at the 1-3 hierarchical level of systemic regulation. At the subordinate 4-6 levels of the hierarchy, the phenomenon of antagonism was also revealed. When regulating systolic (САД) and diastolic (ДАД) blood pressure, this method revealed that nicergoline has a greater effect on the regulation of ДАД.

scholarly journals Insulin resistance, hyperinsulinemia, and obesity-associated hypertension.

1992 ◽  
Vol 3 (5) ◽  
pp. 1064-1077
Author(s):  
M W Brands ◽  
J E Hall
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Insulin Infusion ◽  
Sodium Intake ◽  
Blood Pressure Response ◽  
Peripheral Vascular Resistance ◽  
Peripheral Vascular ◽  
Sustained Increase

Recent work to elucidate the cause of obesity-associated hypertension has focused on insulin resistance and hyperinsulinemia. A significant amount of epidemiologic and correlational evidence suggests a link between these factors and obesity-associated hypertension, and acute insulin infusion studies have revealed renal, neural, and cardiovascular effects of this hormone that, if maintained chronically, could cause hypertension. However, correlations and acute effects may not reliably predict a chronic cause-and-effect relationship, and the fundamental question of whether chronic increases in plasma insulin concentration per se can produce a sustained increase in arterial pressure has not been completely resolved. Recent studies designed to address this question directly have found no evidence of a hypertensive effect of insulin in normal dogs, or in dogs with a 70% reduction in kidney mass and given a high sodium intake. Chronic hyperinsulinemia also did not potentiate the pressor effects of angiotensin II or norepinephrine. In fact, hyperinsulinemia caused significant reductions in total peripheral vascular resistance in dogs and a decrease in arterial pressure. Furthermore, induction of insulin resistance in dogs made obese by being fed a high-fat diet eliminated the decrease in peripheral vascular resistance during chronic insulin infusion but did not uncover a pressor effect of hyperinsulinemia. In contrast, insulin infusion for up to 7 days produced a sustained increase in arterial pressure in rats. Although the mechanism for this pressor response is unknown, these data indicate either that there are major species differences in the chronic blood pressure response to insulin or that specific, presently unknown, conditions must exist in order for insulin to raise blood pressure. Also, it is not clear whether humans respond more like rats or dogs with respect to blood pressure changes during chronic hyperinsulinemia. However, it is apparent that obesity hypertension is probably much too complex to be ascribed to insulin resistance and hyperinsulinemia alone.

Euvolemic cirrhotic dogs in sodium balance maintain normal systemic hemodynamics

1988 ◽  
Vol 66 (1) ◽  
pp. 80-83 ◽  
Author(s):  
M. Levy ◽  
Elizabeth Maher ◽  
Marvin J. Wexler
Keyword(s):  
Cardiac Output ◽  
Liver Function ◽  
Vascular Resistance ◽  
Volume Expansion ◽  
Systemic Hemodynamics ◽  
Peripheral Vascular Resistance ◽  
Sodium Balance ◽  
Biliary Cirrhosis ◽  
Sodium Retention ◽  
Peripheral Vascular

Dogs with chronic biliary cirrhosis and portal hypertension commonly develop plasma volume expansion, urinary sodium retention, ascites, and perturbed systemic hemodynamics, i. e., a rise in cardiac output and a fall in peripheral vascular resistance. Our laboratory has previously demonstrated that creating a side-side portacaval anastomosis in such animals, and so venting hepatoportal pressure, will prevent sodium retention and ascites formation and will maintain the animals euvolemic. In the present study, in four cirrhotic dogs with such an anastomosis, observations made at 12 weeks postbiliary duct ligation, and in the presence of grossly disturbed liver function and morphology, failed to demonstrate any change from control conditions in arterial blood pressure, cardiac output, or peripheral vascular resistance. We conclude that venting hepatoportal pressure in cirrhotic dogs with markedly disturbed liver function prevents the advent of a hyperdynamic circulation, possibly by preventing volume expansion.

Cardiovascular actions of beta-phenylethylamine

1979 ◽  
Vol 236 (4) ◽  
pp. H592-H595
Author(s):  
C. S. Liang ◽  
D. Sprecher
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Left Ventricular ◽  
Peripheral Vascular Resistance ◽  
Adrenergic Nerve ◽  
Peripheral Vascular ◽  
Vascular Effects ◽  
Aortic Blood ◽  
Total Peripheral Vascular Resistance ◽  
Aortic Blood Pressure

beta-Phenylethylamine increased mean aortic blood pressure, total peripheral vascular resistance, left ventricular dP/dt, and (dP/dt)/P in chloralose-anesthetized dogs. Pretreatment with phentolamine reduced the increases in aortic blood pressure and total peripheral vascular resistance produced by beta-phenylethylamine, whereas, the effects of beta-phenylethylamine on left ventricular dP/dt and (dP/dt)/P were abolished by propranolol. beta-Phenylethylamine pretreatment, but increased both after phentolamine pretreatment. Furthermore, both the cardiac and vascular effects of beta-phenylethylamine were abolished by desipramine. These results indicate that beta-phenylethylamine exerts both positive inotropic and vasoconstrictory effects, probably by releasing endogenous norepinephrine from the adrenergic nerve endings.

Coevolution of the rennin–angiotensin system and the nervous control of blood circulation

1984 ◽  
Vol 62 (2) ◽  
pp. 137-147 ◽  
Author(s):  
John X. Wilson
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Renin Angiotensin System ◽  
Peripheral Vascular Resistance ◽  
Peripheral Vascular ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood

The mammalian renin–angiotensin system appears to be involved in the maintenance of blood volume and pressure because (i) sodium depletion, hypovolemia, and hypotension increase renin levels, and (ii) administration of exogenous angiotensin II rapidly increases mineralocorticoid and antidiuretic hormone production, transepithelial ion transport, drinking behavior, and peripheral vascular resistance. Are these also the physiological properties of the renin–angiotensin system in nonmammalian species? Signals for altered levels of renin activity have yet to be conclusively identified in nonmammalian vertebrates, but circulating renin levels are elevated by hypotension in teleost fish and birds. Systemic injection of angiotensin II causes an increase in arterial blood pressure in all the vertebrates studied, suggesting that barostatic control is a universal function of this hormone. Angiotensin II alters vascular tone by direct action on arteriolar muscles in some species, but at concentrations of the hormone which probably are unphysiological. More generally, angiotensin II increases blood pressure indirectly, by acting on the sympathetic nervous system. Catecholamines, derived from chromaffin cells and (or) from peripheral adrenergic nerves, mediate some portion of the vasopressor response to angiotensin II in cyclostomes, elasmobranchs, teleosts, amphibians, reptiles, mammals, and birds. Alteration of sympathetic outflow is a prevalent mechanism through which the renin–angiotensin system may integrate blood volume, cardiac output, and peripheral vascular resistance to achieve control of blood pressure and adequate perfusion of tissues.

Changes in Cardiac Output and Peripheral Vascular Resistance during Weight Training in Athletes

1988 ◽  
Vol 75 (s19) ◽  
pp. 3P-3P ◽  
Author(s):  
LO Hughes ◽  
Mary E Heber ◽  
H Harries ◽  
A Lahiri ◽  
EB Raftery
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Weight Training ◽  
Peripheral Vascular Resistance ◽  
Peripheral Vascular

scholarly journals Features of changes in volume-impedance hemodynamic indicators during the tilt test in young males with a history of vasovagal syncopes

Kardiologiia ◽  
2019 ◽  
Vol 59 (11) ◽  
pp. 31-38
Author(s):  
A. V. Barsukov ◽  
O. G. Chepcheruk ◽  
D. V. Glukhovskoi ◽  
V. V. Yakovlev ◽  
A. V. Gordienko
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Negative Response ◽  
Peripheral Vascular Resistance ◽  
Tilt Test ◽  
Peripheral Vascular ◽  
Total Peripheral Vascular Resistance ◽  
History Of ◽  
Group 3 ◽  
Group 1

Background. The direction of changes in hemodynamic parameters during the tilt test (TT) nin individuals with history of vasovagal syncope (VVS) is a subject of discussion. Objective: to study changes of volume-impedance hemodynamic indicators in the process of tilt test in somatically healthy young men with history of VVS. Materials and methods. A total of 102 men aged 18–30 years were divided into 4 groups, taking into account the specific features of fainting history and response to TT. Persons of group 1 (n=14) had history of VVS and positive response to TT (syncope). Subjects of group 2 (n=14) had history of VVS and a pattern of postural tachycardia without fainting during TT. Persons of group 3 (n=42) had history of VVS and negative response to TT. Subjects of group 4 (n=32) had no history of VVS and negative response to TT. During TT, we studied dynamics of some indicators, including cardiac output (CO) and total peripheral vascular resistance (TPVR). Results. In individuals of all groups in the initial horizontal phase of TT values of CO and TPVR corresponded to the norm. Subjects of group 1 had significantly lower CO compared with subjects of groups 2, 3, 4 (p<0.05, p<0.01, p<0.05, respectively). Values of TPVR in subjects of group 1 were significantly higher than in subjects of groups 2, 3, 4 (p<0.05; p<0.05; p<0.05, respectively). In response to orthostasis CO values increased in groups 1, 2, 4 (by 18%, 10%, 5%, respectively) and did not change in group 3; TPVR values decreased in groups 1, 2 (by 8%, 0.5%, respectively), and increased in groups 3, 4 (by 8%, 4% respectively). In the final horizontal phase of TT, CO values in group 1 were significantly lower than in groups 3, 4 (p<0.05), while TPVR values did not significantly differ between all groups (p>0.05). Conclusions. In tilt-positive and tilt-negative subjects with history of VVS, standardized postural stress leads to unidirectional changes in cardiac output, but to multidirectional changes in total peripheral vascular resistance.

scholarly journals Vascular resistance arm of the baroreflex: methodology and comparison with the cardiac chronotropic arm

2020 ◽  
Vol 128 (5) ◽  
pp. 1310-1320
Author(s):  
J. Krohova ◽  
L. Faes ◽  
B. Czippelova ◽  
R. Pernice ◽  
Z. Turianikova ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Vascular Resistance ◽  
Vascular Tone ◽  
Heart Rate Response ◽  
Peripheral Vascular Resistance ◽  
Noninvasive Measurement ◽  
Peripheral Vascular ◽  
Pressure Changes

Baroreflex response consists of several arms, but the cardiac chronotropic arm (blood pressure changes evoking heart rate response) is usually analyzed. This study introduces a method to assess the vascular baroreflex arm with the continuous noninvasive measurement of peripheral vascular resistance as an output considering causality in the interaction between oscillations and slower dynamics of vascular tone changes. We conclude that although vascular baroreflex arm involvement becomes dominant during orthostasis, gain of this interaction is relatively stable.

Sign in / Sign up

Export Citation Format

Share Document