Effects of Clonidine and Hydrochlorothiazide on the Cardiovascular Response to Mental Stress in Adolescent Hypertension

1982 ◽  
Vol 63 (s8) ◽  
pp. 455s-458s ◽  
Author(s):  
Bonita Falkner ◽  
Gaddo Onesti ◽  
Melton B. Affrime ◽  
David T. Lowenthal
Keyword(s):  
Heart Rate ◽  
Essential Hypertension ◽  
Mental Stress ◽  
Diastolic Pressure ◽  
Cardiovascular Response ◽  
Systolic Pressure ◽  
Cardiovascular Responses ◽  
Plasma Noradrenaline ◽  
Lower Plasma ◽  
Adrenergic Activity

1. The effects of clonidine and hydrochlorothiazide on the cardiovascular responses to mental stess were compared in 29 adolescents with essential hypertension. 2. Clonidine therapy was associated with lower diastolic pressures, heart rate and noradrenaline in response to mental stress. By contrast, hydrochlorothiazide resulted in the reduction of systolic pressure only. The mental stress testing produced a greater absolute diastolic pressure response and higher plasma noradrenaline on hydrochlorothiazide therapy. 3. Juveniles with essential hypertension may be more sensitive to central control of blood pressure and more resistant to diuretics. 4. The reduced diastolic pressure and heart rate response to central stimuli during clonidine therapy may be related to decreased adrenergic activity, as indicated by lower plasma noradrenaline.

Alcohol: Effect on Blood Pressure and Predisposition to Hypertension

1981 ◽  
Vol 61 (s7) ◽  
pp. 373s-375s ◽  
Author(s):  
P. D. Arkwright ◽  
L. J. Beilin ◽  
I. Rouse ◽  
B. K. Armstrong ◽  
R. Vandongen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Essential Hypertension ◽  
Alcohol Consumption ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Threshold Effect ◽  
Health Questionnaire ◽  
Government Employees ◽  
Weekly Alcohol Consumption

1. The association between alcohol consumption and blood pressure was studied in 491 Government employees. The men, aged 21–45 years, volunteered to complete a health questionnaire and submitted to standardized measurements of blood pressure, heart rate and body size. 2. Average weekly alcohol consumption correlated with systolic pressure (r = 0.18, P < 0.001) but not with diastolic pressure. Systolic pressure increased progressively with increasing alcohol consumption with no obvious threshold effect. The effect of alcohol was independent of age, obesity (Quetelet's index) or cigarette smoking. 3. Results indicate that alcohol ranks close to obesity as a preventable cause of essential hypertension in the community.

Cardiac Baroreflex during the Postoperative Period in Patients with Hypertension 

1999 ◽  
Vol 90 (3) ◽  
pp. 681-692 ◽  
Author(s):  
Joel L. Parlow ◽  
Gerard Begou ◽  
Pierre Sagnard ◽  
Jean Marie Cottet-Emard ◽  
Jean Claude Levron ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Essential Hypertension ◽  
Rate Control ◽  
Diastolic Pressure ◽  
Elective Surgery ◽  
Recovery Period ◽  
Systolic Pressure ◽  
Heart Rate Control ◽  
Baroreflex Control

Background Patients with essential hypertension show altered baroreflex control of heart rate, and during the perioperative period they demonstrate increased circulatory instability. Clonidine has been shown to reduce perioperative circulatory instability. This study documents changes in measures of heart rate control after surgery in patients with essential hypertension and determines the effects of clonidine on postoperative heart rate control in these patients. Methods Using a randomized double-blind placebo-controlled design, 20 patients with essential hypertension (systolic pressure >160 mm Hg or diastolic pressure >95 mm Hg for > or =1 yr) were assigned to receive clonidine (or placebo), 6 microg/kg orally 120 min before anesthesia and 3 microg/kg intravenously over 60 min before the end of surgery. The spontaneous baroreflex ("sequence") technique and analysis of heart rate variability were used to quantify control of heart rate at baseline, before induction of anesthesia, and 1 and 3 h postoperatively. Results Baroreflex slope and heart rate variability were reduced postoperatively in patients given placebo but not those given clonidine. Clonidine resulted in greater postoperative baroreflex slope and power at all frequency ranges compared with placebo (4.9+/-2.9 vs. 2.2+/-2.1 ms/mm Hg for baroreflex slope, 354+/-685 vs. 30+/-37 ms2/Hz for high frequency variability). Clonidine also resulted in lower concentrations of catecholamine, decreased mean heart rate and blood pressure, and decreased perioperative tachycardia and hypertension. Conclusions Patients with hypertension exhibit reduced heart rate control during the recovery period after elective surgery. Clonidine prevents this reduction in heart rate control. This may represent a basis for the improved circulatory stability seen with perioperative administration of clonidine.

The Effects of Cardioselective and Non-Selective β-Adrenoceptor Blockade on the Hypokalaemic and Cardiovascular Responses to Adrenomedullary Hormones in Man

1983 ◽  
Vol 65 (2) ◽  
pp. 143-147 ◽  
Author(s):  
A. D. Struthers ◽  
J. L. Reid ◽  
R. Whitesmith ◽  
J. C. Rodger
Keyword(s):  
Heart Rate ◽  
Serum Potassium ◽  
Qt Interval ◽  
Diastolic Pressure ◽  
Plasma Concentrations ◽  
Systolic Pressure ◽  
Cardiovascular Responses ◽  
Potassium Influx ◽  
Adrenomedullary Hormones ◽  
Stimulation Of

1. Adrenaline was infused intravenously in nine normal volunteers to plasma concentrations similar to those found after myocardial infarction. This study was undertaken on three occasions after 5 days' treatment with placebo or the β-adrenoceptor antagonists, atenolol or timolol. 2. Adrenaline increased the systolic pressure by 11 mmHg, decreased the diastolic pressure by 14 mmHg, and increased the heart rate by 7 beats/min. These changes were prevented by atenolol. However, after timolol the diastolic pressure rose (+19 mmHg) and heart rate fell (− 8 beats/min). 3. Adrenaline caused the corrected QT interval (QTc) to lengthen (0.36 ± 0.02 s to 0.41 ± 0.06 s). No significant changes were found in the QTc when subjects were pretreated with atenolol or timolol. 4. The serum potassium fell from 4.06 to 3.22 mmol/l after adrenaline. Serum potassium fell to a lesser extent to 3.67 mmol/l after atenolol and actually increased to 4.25 mmol/l after timolol. Adrenaline-mediated hypokalaemia appears to result from the stimulation of a β2-adrenoceptor linked to membrane Na+/K+-ATPase causing potassium influx.

Acute manipulations of plasma volume alter arterial pressure responses during Valsalva maneuvers

1999 ◽  
Vol 86 (6) ◽  
pp. 1852-1857 ◽  
Author(s):  
Janice M. Fritsch-Yelle ◽  
Victor A. Convertino ◽  
Todd T. Schlegel
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Phase Ii ◽  
Plasma Volume ◽  
Diastolic Pressure ◽  
Valsalva Maneuver ◽  
Isotonic Saline ◽  
Systolic Pressure ◽  
Cardiovascular Responses ◽  
Phase Iii

The effects of changes in blood volume on arterial pressure patterns during the Valsalva maneuver are incompletely understood. In the present study we measured beat-to-beat arterial pressure and heart rate responses to supine Valsalva maneuvers during normovolemia, hypovolemia induced with intravenous furosemide, and hypervolemia induced with ingestion of isotonic saline. Valsalva responses were analyzed according to the four phases as previously described (W. F. Hamilton, R. A. Woodbury, and H. T. Harper, Jr. JAMA 107: 853–856, 1936; W. F. Hamilton, R. A. Woodbury, and H. T. Harper, Jr. Am. J. Physiol. 141: 42–50, 1944). Phase I is the initial onset of straining, which elicits a rise in arterial pressure; phase II is the period of straining, during which venous return is impeded and pressure falls (early) and then partially recovers (late); phase III is the initial release of straining; and phase IV consists of a rapid “overshoot” of arterial pressure after the release. During hypervolemia, early phase II arterial pressure decreases were significantly less than those during hypovolemia, thus making the response more “square.” Systolic pressure hypervolemic vs. hypovolemic falls were −7.4 ± 2.1 vs. −30.7 ± 7 mmHg ( P = 0.005). Diastolic pressure hypervolemic vs. hypovolemic falls were −2.4 ± 1.6 vs. −15.2 ± 2.6 mmHg ( P = 0.05). A significant direct correlation was found between plasma volume and phase II systolic pressure falls, and a significant inverse correlation was found between plasma volume and phase III-IV systolic pressure overshoots. Heart rate responses to systolic pressure falls during phase II were significantly less during hypovolemia than during hypervolemia (0.7 ± 0.2 vs. 2.82 ± 0.2 beats ⋅ min−1 ⋅ mmHg−1; P = 0.05) but were not different during phase III-IV overshoots. We conclude that acute changes in intravascular volume from hypovolemia to hypervolemia affect cardiovascular responses, particularly arterial pressure changes, to the Valsalva maneuver and should be considered in both clinical and research applications of this maneuver.

Renal and cardiovascular effects of caffeine: A dose–response study

1987 ◽  
Vol 72 (6) ◽  
pp. 749-756 ◽  
Author(s):  
A. P. Passmore ◽  
G. B. Kondowe ◽  
G. D. Johnston
Keyword(s):  
Heart Rate ◽  
Diastolic Pressure ◽  
Renal Plasma Flow ◽  
Urine Volume ◽  
Systolic Pressure ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Plasma Noradrenaline ◽  
Dose Response Study

1. The effects of increasing oral doses of caffeine (45, 90, 180 and 360 mg) on effective renal plasma flow (ERPF), plasma renin activity (PRA), serum electrolytes, plasma noradrenaline, blood pressure and heart rate were studied in eight healthy male volunteers. 2. Urine volume was increased by 360 mg of caffeine only. At caffeine doses greater than 90 mg urinary sodium excretion was significantly increased. There were no changes in ERPF. 3. Serum potassium was significantly reduced by 360 mg of caffeine. 4. Caffeine increased systolic pressure in a dose related manner. Diastolic pressure was also increased, but not in relation to dose. A 360 mg dose of caffeine produced a late increase in heart rate. These changes were not associated with any alterations in PRA or in plasma noradrenaline.

Control circulatory values of morphinepentobarbitalized dogs

1960 ◽  
Vol 199 (5) ◽  
pp. 797-799 ◽  
Author(s):  
S. Deavers ◽  
E. L. Smith ◽  
R. A. Huggins
Keyword(s):  
Heart Rate ◽  
Body Weight ◽  
Cell Volume ◽  
Blood Volume ◽  
Plasma Volume ◽  
Protein Concentration ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Control Data ◽  
Plasma Protein Concentration

Mean control data on a series of 100 dogs are presented. Cell volume, measured with Cr51-tagged red cells and plasma volume determined simultaneously by T-1824 dye was 33.5 ± 0.74 cc/kg and 50.2 ± 1.11 cc/kg, respectively. The venous hematocrit was 45.2% and the circulatory/venous hematocrit ratio was 0.89 ± 0.01 for the group. The plasma protein concentration of these animals was 6.25 ± 0.07 gm/100 cc. No difference in blood volume per unit of body weight was found between large (12.6 kg) and small (5.8 kg) dogs. The femoral mean systolic pressure was 139.0 ± 2.53 mm Hg, the diastolic pressure 65.6 ± 1.46 mm Hg and the heart rate 85.9 ± 2.86/min.

Effect of sleep restriction on orthostatic cardiovascular control in humans

2000 ◽  
Vol 88 (3) ◽  
pp. 966-972 ◽  
Author(s):  
N. K. Muenter ◽  
D. E. Watenpaugh ◽  
W. L. Wasmund ◽  
S. L. Wasmund ◽  
S. A. Maxwell ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Lower Body Negative Pressure ◽  
Systolic Pressure ◽  
Cardiovascular Responses ◽  
Sleep Restriction ◽  
Orthostatic Tolerance ◽  
Arterial Baroreflex ◽  
Finger Arterial Pressure ◽  
Before And After

We hypothesized that sleep restriction (4 consecutive nights, 4 h sleep/night) attenuates orthostatic tolerance. The effect of sleep restriction on cardiovascular responses to simulated orthostasis, arterial baroreflex gain, and heart rate variability was evaluated in 10 healthy volunteers. Arterial baroreflex gain was determined from heart rate responses to nitroprusside-phenylephrine injections, and orthostatic tolerance was tested via lower body negative pressure (LBNP). A Finapres device measured finger arterial pressure. No difference in baroreflex function, heart rate variability, or LBNP tolerance was observed with sleep restriction ( P > 0.3). Systolic pressure was greater at −60 mmHg LBNP after sleep restriction than before sleep restriction (110 ± 6 and 124 ± 3 mmHg before and after sleep restriction, respectively, P = 0.038), whereas heart rate decreased (108 ± 8 and 99 ± 8 beats/min before and after sleep restriction, respectively, P = 0.028). These data demonstrate that sleep restriction produces subtle changes in cardiovascular responses to simulated orthostasis, but these changes do not compromise orthostatic tolerance.

Reflex cardiovascular response to exercise is modulated by circulating vasopressin

1992 ◽  
Vol 263 (5) ◽  
pp. R1104-R1109 ◽  
Author(s):  
C. L. Stebbins
Keyword(s):  
Heart Rate ◽  
Receptor Antagonist ◽  
Cardiovascular Response ◽  
Regional Blood Flow ◽  
Plasma Concentrations ◽  
Cardiovascular Responses ◽  
Vascular Effect ◽  
Ganglionic Blockade ◽  
Hindlimb Muscles ◽  
Before And After

Peripheral vasopressin (AVP) can act centrally to sensitize the arterial baroreflex and/or peripherally to attenuate regional blood flow by a direct vascular effect. Because plasma concentrations of AVP increase during exercise, this study examined the possibility that AVP is capable of modulating the reflex cardiovascular response to static muscle contraction. Thus, in anesthetized cats, the pressor [mean arterial pressure (MAP)], myocardial contractile (dP/dt), and heart rate responses to 30-45 s of electrically induced static contraction of the hindlimb muscles were compared before and after intravenous injection of the V1 receptor antagonist d[CH2)5Tyr(Me)]-AVP (V1-x, n = 7), V1-x plus the V2 receptor antagonist [d(CH2)5,D-Phe2,Ile4,Arg8,Ala9]vasopressin (V2-x, n = 5), or the ganglionic blocker hexamethonium chloride (n = 5). In three additional cats, the contraction-induced cardiovascular response was monitored before and after injection of V1-x + V2-x and after hexamethonium. Subsequent to treatment with V1-x, the MAP and dP/dt responses to contraction were augmented by 18 +/- 5 and 22 +/- 10%, respectively (P < 0.05). After injection of V1-x + V2-x, the MAP and dP/dt responses were augmented to a similar extent (32 +/- 6 and 40 +/- 17%, respectively; P < 0.05). However, there was no difference in the magnitude of augmentation of these responses between the two conditions. The heart rate response was not altered by either treatment. Ganglionic blockade eliminated the cardiovascular responses to contraction. Last, when the pressor and contractile responses to contraction were initially augmented by administration of V1-x + V2-x, subsequent ganglionic blockade abolished the entire cardiovascular response.(ABSTRACT TRUNCATED AT 250 WORDS)

Modulation of cardiovascular response to dynamic exercise by fastigial nucleus

1984 ◽  
Vol 56 (5) ◽  
pp. 1369-1377 ◽  
Author(s):  
K. J. Dormer
Keyword(s):  
Blood Pressure ◽  
Repeated Measures ◽  
Cardiovascular Response ◽  
Systolic Pressure ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Fastigial Nucleus ◽  
Ventricular Systolic Pressure ◽  
Arterial Blood

Mongrel dogs (n = 34) were used to record the cardiovascular responses during submaximal exercise-tolerance tests (ETT) before and after the placement of lesions in rostral portions of the cerebellar fastigial nucleus (FN). Sterile surgical procedures were used to implant solid-state pressure transducers into the left ventricle or descending aorta (anesthesia 1% halothane in O2) and multipolar stainless steel electrodes into FN (anesthesia alpha-chloralose 115 mg/kg iv). Heart rate (HR), maximal left ventricular systolic pressure ( LVPmax ) and its first derivative ( dLVP /dt), and mean arterial blood pressure (MAP) were recorded during a motorized treadmill ETT. Electrolytic direct-current or radio-frequency lesions were made through the indwelling FN electrodes, and the ETT was repeated following 10–14 days recovery. Two-way analysis of variance (ANOVA), with repeated measures on one, and one-way ANOVA for simple effects indicated a significant reduction in HR and MAP (P less than 0.01) but not LVPmax and dLVP /dt occurred during exercise as a result of rostral FN lesions. Although the trend for reduced LVPmax and dLVP /dt was also evident, a relatively greater decrease in blood pressure occurred in the peripheral vasculature during exercise. It was concluded that FN acts as a modulator of HR and MAP during dynamic exercise because of the observed deficits, and because FN is known to both send efferent projections to medullary vasomotor areas and receive projections from motor cortex and muscle and joint afferents.

Cardiovascular Responses to Submaximal Concentric and Eccentric Isokinetic Exercise in Older Adults

1999 ◽  
Vol 7 (1) ◽  
pp. 20-31 ◽  
Author(s):  
Elizabeth Thompson ◽  
Theo H. Versteegh ◽  
Tom J. Overend ◽  
Trevor B. Birmingham ◽  
Anthony A. Vandervoort
Keyword(s):  
Older Adults ◽  
Heart Rate ◽  
Perceived Exertion ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Knee Extension ◽  
Resistance Testing ◽  
Exercise Heart Rate ◽  
Arterial Blood ◽  
S Peak

Our purpose was to describe heart rate (HR), mean arterial blood pressure (MAP), and perceived exertion (RPE) responses to submaximal isokinetic concentric (CON) and eccentric (ECC) exercise at the same absolute torque output in older adults. Peak torques for ECC and CON knee extension were determined in healthy older males (n = 13) and females (n = 7). Subjects then performed separate, randomly ordered, 2-min bouts of CON and ECC exercise. Heart rate and MAP increased (p < .001) from resting values throughout both exercise bouts. CON exercise elicited a significantly greater cardiovascular response than ECC exercise after 60 s. Peak HR, MAP, and RPE after CON exercise were greater than after ECC exercise (p < .01). At the same absolute torque output, isokinetic CON knee extension exercise resulted in a significantly greater level of cardiovascular stress than ECC exercise. These results are relevant to resistance testing and exercise in older people.

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