Effects of Prizidilol (SKF 92657) on Blood Pressure, Haemodynamics, Sympathetic Nervous System Activity and Plasma Volume in Essential Hypertension

1981 ◽  
Vol 61 (s7) ◽  
pp. 465s-468s ◽  
Author(s):  
R. Fariello ◽  
C. L. Alicandri ◽  
E. Agabiti-Rosei ◽  
G. Romanelli ◽  
M. Castellano ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Volume ◽  
Antihypertensive Effect ◽  
Blood Pressure Reduction ◽  
Cardiac Performance ◽  
Plasma Aldosterone ◽  
Nervous System Activity ◽  
Peripheral Vasodilatation ◽  
Noradrenaline And Adrenaline

1. The antihypertensive effect of 4 weeks' treatment with prizidilol (SKF 92657) (mean dosage 520 mg once or twice daily) was studied in ten essential hypertensive patients. 2. Both systolic and diastolic blood pressure were significantly reduced in all cases. Supine heart rate did not change, and in the erect position heart rate was significantly lowered. 3. Blood pressure reduction was due to peripheral vasodilatation, as the cardiac index increased after 4 weeks of prizidilol treatment. 4. After prizidilol plasma noradrenaline and adrenaline increased significantly, and PRA and plasma aldosterone were reduced. Although plasma volume increased, body weight did not change. 5. Cardiac performance, as evaluated by the PEP/LVET ratio, improved after treatment with prizidilol.

Dose-Response Curve and Time Course of the Antihypertensive Effect of SKF 92 657, a β-Receptor-Blocking and Vasodilating Compound

1980 ◽  
Vol 59 (s6) ◽  
pp. 461s-463s ◽  
Author(s):  
G. Leonetti ◽  
Laura Terzoli ◽  
Carla Sala ◽  
C. Bianchini ◽  
A. Zanchetti
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Response Curve ◽  
Time Course ◽  
Antihypertensive Effect ◽  
Blood Pressure Reduction ◽  
Dynamic Exercise ◽  
Β Receptor ◽  
Oral Doses ◽  
Uniform Reduction

1. The antihypertensive effect of the new drug, SKF 92 657, a hydrazinopyridazine derivative, possessing both β-adrenoreceptor-blocking and vasodilating properties, was investigated in essential hypertension. 2. Single oral doses of 1.0 or 2.0 mg/kg did not produce any consistent decrease in blood pressure; 4.0 mg/kg was the threshold dose for a mild but not significant blood pressure reduction, whereas 8.0 mg/kg caused a significant and marked blood pressure decrease without clinically relevant changes in heart rate. 3. Continued administration of the drug for 7 days induced a significant and uniform reduction in blood pressure without tachycardia. The increase in systolic blood pressure and in heart rate caused by dynamic exercise was left unaffected by the drug.

Ruta montana evokes antihypertensive activity through increase of prosta-glandins release in L-NAME-induced hypertensive rats

2020 ◽  
Vol 20 ◽  
Author(s):  
El-Ouady Fadwa ◽  
Mohamed Eddouks
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Aqueous Extract ◽  
Antihypertensive Effect ◽  
Antihypertensive Activity ◽  
Computer Assisted ◽  
Hypertensive Rats ◽  
Vasorelaxant Effect ◽  
Vasorelaxant Activity ◽  
Ruta Montana

Aims: The aim of the study was to investigate experimentally the antihypertensive effect of Ruta Montana. Background: Ruta montana L. is traditionally used in Moroccan herbal medicine to treat hypertension. This study aimed to evaluate experimentally the hypotensive and vasoactive properties of this plant. Objective: The objective of the study was to evaluate the effect of the aqueous extract of Ruta Montana on blood pressure parameters in LNAME-induced hypertensive rats and to determine the vasorelaxant activity of this aqueous extract. Methods: The antihypertensive effect of the aqueous extract obtained from Ruta montana aerial parts (RMAPAE) (200 mg/kg) was evaluated in normal and anesthetized hypertensive rats. Blood pressure parameters (systolic blood pressure (SBP), mean blood pressure (MBP) and diastolic blood pressure (DBP)) and heart rate were measured using a tail-cuff and a computer-assisted monitoring device. The acute and chronic effect of RMAPAE was recorded during 6 hours for the acute experiment and during 7 days for the sub-chronic test. In the other set, the vasorelaxant effect of RMAPAE on the contractile response was undertaken in isolated thoracic aorta. Results: The results indicated that RMAPAE extract significantly decreased SBP, MBP, DBP and heart rate in L-NAMEinduced hypertensive rats. Furthermore, RMAPAE was demonstrated to induce a dose dependent relaxation in the aorta precontracted with Epinephrine or KCl. More interestingly, this vasorelaxant activity of RMAPAE seems to be probably mediated through the prostaglandins pathway. Conclusion: The present study illustrates the beneficial action of Ruta montana on hypertension and supports then its use as an antihypertensive agent.

Antihypertensive Property and Renal Protection by Shichimotsu-koka-to Extract in Salt-induced Hypertension in Dahl Strain Rats

1994 ◽  
Vol 22 (01) ◽  
pp. 51-62 ◽  
Author(s):  
Nobuhito Hiwara ◽  
Yoshio Uehara ◽  
Satoru Takada ◽  
Yukari Kawabata ◽  
Nobuko Ohshima ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Aortic Wall ◽  
Antihypertensive Effect ◽  
Blood Pressure Reduction ◽  
Glomerular Sclerosis ◽  
Pressure Reduction ◽  
Renal Protection ◽  
Induced Hypertension ◽  
Sclerotic Lesions

We determined whether or not the kampo formula, Shichimotsu-koka-to extract, attenuates the development of salt-induced hypertension and provides renal protection against hypertensive injury in Dahl salt-sensitive (Dahl S) rats. A six-week treatment using this formula dose-dependently decreased the systolic blood pressure in Dahl S rats fed a high-salt (2% NaCl) diet. This blood pressure reduction was associated with a decrease in the thickness of the aortic wall. Renal function was not altered with this treatment; however, glomerular sclerotic lesions in the kidney were significantly attenuated. Neither arterial nor tubular lesions were affected. These data suggest that Shichimotsu-koka-to extract exhibits an antihypertensive effect which is associated with partial resolution of glomerular sclerosis in the kidney.

Effect of Baroreceptor Deafferentation on Central Catecholamines in the Rat

1979 ◽  
Vol 57 (s5) ◽  
pp. 221s-223s ◽  
Author(s):  
Margaret A. Petty ◽  
J. P. Chalmers ◽  
M. Brown ◽  
J. L. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Tyrosine Hydroxylase ◽  
Brain Stem ◽  
Hydroxylase Activity ◽  
Methyltransferase Activity ◽  
Neurogenic Hypertension ◽  
Noradrenaline Synthesis ◽  
Noradrenaline And Adrenaline ◽  
Sympathetic Efferent Activity

1. Sinoaortic deafferentation in the rat leads to increased blood pressure and heart rate. 2. Early increases in tyrosine hydroxylase activity both in brain stem and hypothalamus suggest that increased noradrenaline synthesis may contribute to the development of neurogenic hypertension. 3. After 4 weeks, phenylethanolamine-N-methyltransferase activity was reduced in the hypothalamus. 4. Noradrenaline- and adrenaline, but not dopamine-containing neurones may participate in regulation of sympathetic efferent activity.

Measurement of sympathetic nerve activity in the unanesthetized rat

1989 ◽  
Vol 67 (1) ◽  
pp. 250-255 ◽  
Author(s):  
J. P. Fluckiger ◽  
G. Gremaud ◽  
B. Waeber ◽  
A. Kulik ◽  
A. Ichino ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Blood Pressure Reduction ◽  
Response Curves ◽  
Nerve Activity ◽  
Dose Dependent

A new system was developed in our laboratory to continuously monitor intra-arterial pressure, heart rate, and sympathetic nerve activity in unanesthetized rats. The animals were prepared 24 h before the start of the experiments. Sympathoneural traffic was measured at the level of splanchnic nerve. The amplitude of the spikes recorded at this level was utilized to express sympathetic nerve activity. The amplitude of the residual electroneurogram signal present 30 min after the rats were killed was 32 +/- 2 mV (mean +/- SE; n = 11). For analysis, these background values were subtracted from values determined in vivo. The nerve we studied contains postganglionic fibers, since electrical activity decreased in response to ganglionic blockade with pentolinium (1.25 mg/min iv for 4 min). The amplitude of spikes fell by 43 +/- 4% (n = 4). Sympathetic nerve activity was highly reproducible at a 24-h interval (104 +/- 26 vs. 111 +/- 27 mV for the amplitude of spikes; n = 11). Dose-response curves to the alpha 1-stimulant methoxamine and to bradykinin were established in four rats. The increase in blood pressure induced by methoxamine caused a dose-dependent fall in sympathetic nerve activity, whereas the blood pressure reduction resulting from bradykinin was associated with a dose-dependent activation of sympathetic drive. These data therefore indicate that it is possible with out system to accurately measure sympathetic nerve activity in the awake rat, together with intra-arterial pressure and heart rate.

Effect of head-down-tilt bed rest and hypovolemia on dynamic regulation of heart rate and blood pressure

2000 ◽  
Vol 279 (6) ◽  
pp. R2189-R2199 ◽  
Author(s):  
Ken-Ichi Iwasaki ◽  
Rong Zhang ◽  
Julie H. Zuckerman ◽  
James A. Pawelczyk ◽  
Benjamin D. Levine
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Transfer Function ◽  
Stroke Volume ◽  
Plasma Volume ◽  
High Frequency ◽  
Function Analysis ◽  
Bed Rest ◽  
Baroreflex Control ◽  
Transfer Function Analysis

Adaptation to head-down-tilt bed rest leads to an apparent abnormality of baroreflex regulation of cardiac period. We hypothesized that this “deconditioning response” could primarily be a result of hypovolemia, rather than a unique adaptation of the autonomic nervous system to bed rest. To test this hypothesis, nine healthy subjects underwent 2 wk of −6° head-down bed rest. One year later, five of these same subjects underwent acute hypovolemia with furosemide to produce the same reductions in plasma volume observed after bed rest. We took advantage of power spectral and transfer function analysis to examine the dynamic relationship between blood pressure (BP) and R-R interval. We found that 1) there were no significant differences between these two interventions with respect to changes in numerous cardiovascular indices, including cardiac filling pressures, arterial pressure, cardiac output, or stroke volume; 2) normalized high-frequency (0.15–0.25 Hz) power of R-R interval variability decreased significantly after both conditions, consistent with similar degrees of vagal withdrawal; 3) transfer function gain (BP to R-R interval), used as an index of arterial-cardiac baroreflex sensitivity, decreased significantly to a similar extent after both conditions in the high-frequency range; the gain also decreased similarly when expressed as BP to heart rate × stroke volume, which provides an index of the ability of the baroreflex to alter BP by modifying systemic flow; and 4) however, the low-frequency (0.05–0.15 Hz) power of systolic BP variability decreased after bed rest (−22%) compared with an increase (+155%) after acute hypovolemia, suggesting a differential response for the regulation of vascular resistance (interaction, P < 0.05). The similarity of changes in the reflex control of the circulation under both conditions is consistent with the hypothesis that reductions in plasma volume may be largely responsible for the observed changes in cardiac baroreflex control after bed rest. However, changes in vasomotor function associated with these two conditions may be different and may suggest a cardiovascular remodeling after bed rest.

scholarly journals Deficiency of T-type Ca2+ channels Cav3.1 and Cav3.2 has no effect on angiotensin II-induced hypertension but differential effect on plasma aldosterone in mice

2019 ◽  
Vol 317 (2) ◽  
pp. F254-F263
Author(s):  
Anne D. Thuesen ◽  
Stine H. Finsen ◽  
Louise L. Rasmussen ◽  
Ditte C. Andersen ◽  
Boye L. Jensen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Natriuretic Peptide ◽  
Mineralocorticoid Receptor ◽  
Plasma Aldosterone ◽  
Receptor Blocker ◽  
Ang Ii ◽  
Induced Hypertension

T-type Ca2+ channel Cav3.1 promotes microvessel contraction ex vivo. It was hypothesized that in vivo, functional deletion of Cav3.1, but not Cav3.2, protects mice against angiotensin II (ANG II)-induced hypertension. Mean arterial blood pressure (MAP) and heart rate were measured continuously with chronically indwelling catheters during infusion of ANG II (30 ng·kg−1·min−1, 7 days) in wild-type (WT), Cav3.1−/−, and Cav3.2−/− mice. Plasma aldosterone and renin concentrations were measured by radioimmunoassays. In a separate series, WT mice were infused with ANG II (100 ng·kg−1·min−1) with and without the mineralocorticoid receptor blocker canrenoate. Cav3.1−/− and Cav3.2−/− mice exhibited no baseline difference in MAP compared with WT mice, but day-night variation was blunted in both Cav3.1 and Cav3.2−/− mice. ANG II increased significantly MAP in WT, Cav3.1−/−, and Cav3.2−/− mice with no differences between genotypes. Heart rate was significantly lower in Cav3.1−/− and Cav3.2−/− mice compared with control mice. After ANG II infusion, plasma aldosterone concentration was significantly lower in Cav3.1−/− compared with Cav3.2−/− mice. In response to ANG II, fibrosis was observed in heart sections from both WT and Cav3.1−/− mice and while cardiac atrial natriuretic peptide mRNA was similar, the brain natriuretic peptide mRNA increase was mitigated in Cav3.1−/− mice ANG II at 100 ng/kg yielded elevated pressure and an increased heart weight-to-body weight ratio in WT mice. Cardiac hypertrophy, but not hypertension, was prevented by the mineralocorticoid receptor blocker canrenoate. In conclusion, T-type channels Cav3.1and Cav3.2 do not contribute to baseline blood pressure levels and ANG II-induced hypertension. Cav3.1, but not Cav3.2, contributes to aldosterone secretion. Aldosterone promotes cardiac hypertrophy during hypertension.

Renin and Aldosterone Release during Sympathetic Stimulation in Tetraplegia

1981 ◽  
Vol 60 (4) ◽  
pp. 399-404 ◽  
Author(s):  
C. J. Mathias ◽  
H. L. Frankel ◽  
I. B. Davies ◽  
V. H. T. James ◽  
W. S. Peart
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Renin Activity ◽  
Diastolic Blood Pressure ◽  
Pressor Response ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Sympathetic Stimulation

1. The effect of endogenous sympathetic stimulation (induced by urinary bladder stimulation) and intravenous infusion of noradrenaline and isoprenaline on blood pressure, heart rate and levels of plasma renin activity and plasma aldosterone were studied in six tetraplegic patients. Data from infusion studies were compared with data from six normal subjects studied in an identical manner. 2. Bladder stimulation in the tetraplegic patients caused a marked rise in blood pressure and fall in heart rate, but no change in plasma renin activity or plasma aldosterone. 3. Noradrenaline infusion resulted in an enhanced pressor response in the tetraplegic patients when compared with the normal subjects. Heart rate fell in both groups. Plasma renin activity and plasma aldosterone did not change in either group. 4. Isoprenaline infusion caused a fall in both systolic and diastolic blood pressure in the tetraplegic patients, unlike the normal subjects in whom there was a rise in systolic and a fall in diastolic blood pressure. Heart rate and plasma renin activity rose in both groups. Plasma aldosterone did not change in either group. 5. We conclude that in tetraplegic patients neither endogenous sympathetic stimulation by bladder stimulation nor infusion of noradrenaline raises plasma renin activity. Isoprenaline increases plasma renin activity to the same extent as in normal subjects. Renin release mechanisms in tetraplegic patients therefore do not appear to be hypersensitive to catecholamines. Plasma aldosterone is not influenced by any of the stimuli.

Antihypertensive Effect of Guanfacine: Long-Term ‘Once-a-Day’ Treatment and Sudden Withdrawal

1981 ◽  
Vol 61 (s7) ◽  
pp. 469s-471s
Author(s):  
I. Szám ◽  
J. Holló
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Antihypertensive Effect ◽  
Clinical Symptoms ◽  
Day Treatment ◽  
Pressure Rise ◽  
Common Side Effect ◽  
Blood Pressure Rise ◽  
Abrupt Discontinuation

1. Twenty patients with essential hypertension were treated with guanfacine given in single daily doses of 1–5 mg over a period of 24 weeks. Compared with the initial values at the end of the first wash-out period, there was a significant decrease of blood pressure and heart rate. The most common side effect, dryness of the mouth, usually disappeared after 8–10 weeks of treatment. No changes in laboratory values were seen. In the post-treatment placebo period there were significant increases in blood pressure and heart rate compared with the last readings during the treatment period. However, these never exceeded the pretreatment values. 2. In a second trial guanfacine (1–5 mg daily) was abruptly discontinued in 11 patients after 6–20 weeks' treatment. Blood pressure was measured twice a day, in lying and standing positions, during the 4 days before abrupt withdrawal of guanfacine and for 7 days after discontinuation. Clopamide was given concurrently to two patients, and this was continued after withdrawal of guanfacine. Only in two patients did the blood pressure rise to values above the initial levels (30 mmHg systolic and 10 mmHg diastolic), but no clinical symptoms were observed during the withdrawal. A transitory increase of heart rate of between 10 and 30 beats/min was observed in five patients after abrupt discontinuation of the drug.

Effects of opioid antagonism on the haemodynamic and hormonal responses to exercise

1988 ◽  
Vol 75 (3) ◽  
pp. 293-300 ◽  
Author(s):  
Jan Staessen ◽  
Roberto Fiocchi ◽  
Roger Bouillon ◽  
Robert Fagard ◽  
Peter Hespel ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Serum Insulin ◽  
Plasma Renin ◽  
Endogenous Opioids ◽  
Renin Activity ◽  
Plasma Adrenaline ◽  
Noradrenaline And Adrenaline

1. Physical effort involves, along with an increase in the plasma concentration of β-endorphin, profound adaptations of the circulation and the endocrine system. The effects of opioid antagonism on the responses of blood pressure, heart rate and several hormones to exercise were therefore studied in 10 normal men. They exercised in the supine position up to 33% and 66% of their maximal exercise capacity and received in a randomized double-blind cross-over protocol, either saline or naloxone (10 mg intravenously, followed by a continuous infusion of 10 mg/h). 2. Intra-arterial pressure and heart rate were continuously monitored, but were not affected by naloxone. 3. At rest, opioid antagonism produced a rise in plasma renin activity and in plasma adrenocorticotropin, Cortisol and aldosterone, but only the stimulation of the two adrenocortical hormones differed significantly from the control experiments; at rest naloxone also prevented the fall in plasma adrenaline, which occurred with saline infusion. Furthermore, the exercise-induced rises in plasma angiotensin II, aldosterone, Cortisol, noradrenaline and adrenaline were higher on naloxone than on saline, while a similar tendency was also present for the increases with exercise in plasma renin activity and plasma adrenocorticotropin. Neither at rest nor during exercise did opioid antagonism alter plasma lactate and glucose and serum insulin and growth hormone. 4. In conclusion, (1) endogenous opioids are not involved in the responses of blood pressure and heart rate to supine exercise; (2) at rest and during exercise, the endogenous opioids inhibit the secretion of adrenocorticotropin, aldosterone, Cortisol, noradrenaline and adrenaline; (3) they also inhibit the plasma renin-angiotensin II system indirectly via the catecholamines.

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