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PubMed1990

Atrial natriuretic peptide infusion causes vasoconstriction after autonomic blockade in conscious dogs.

Many studies have shown that atrial natriuretic peptide (ANP) reduces mean arterial pressure (MAP) in conscious animals by lowering cardiac output (CO) with no change or even increased total peripheral resistance (TPR). Because ANP is thought to be a vasodilator, the lack of fall in TPR in conscious animals is generally considered to be due to autonomic reflex increases in vascular resistance. In the present study in conscious, trained, chronically instrumented dogs (n = 7), we measured hemodynamic and renal excretory responses to 30-min infusions of alpha-human ANP (alpha hANP; 25, 50, and 100 ng.kg-1.min-1) in the presence and absence of autonomic nervous system blockade using the ganglion blocking agent pentolinium. In the absence of blockade, MAP and CO fell, whereas TPR rose with alpha hANP infusions, but these changes did not reach significance. There were significant increases in renal vascular resistance (RVR; 16-25%) and mesenteric vascular resistance (MVR; 14-40%). During autonomic nervous system blockade, alpha hANP caused dose-related reductions in MAP (7-12%), due to falls in CO (13-34%). Remarkably, the absence of autonomic reflex responses exposed substantial dose-related increases in TPR (5-33%). Autonomic blockade did not alter the ANP-induced increases in MVR but did abolish the rises in RVR. In summary, ANP caused vasoconstriction in mesenteric vasculature and substantial vasoconstriction in other nonrenal areas, independent of autonomic reflexes.

Animals↗

PubMed1996

Cardiac output and renal function during insulin hypertension in Sprague-Dawley rats.

Hyperinsulinemia has been reported to cause hypertension in rats; however, the renal and hemodynamic mechanisms are not known. In this study, changes in renal function, cardiac output (CO), and total peripheral resistance (TPR) were measured during chronic insulin infusion in eight rats (approximately 350 g). After a 4-day control period, a 7-day insulin infusion was begun (1.5 mU.kg-1.min-1 iv), together with glucose (22 mg.kg-1.min-1 iv) to prevent hypoglycemia. Mean arterial pressure (MAP), CO, TPR, and heart rate were measured 24 h/day. MAP increased from 92 +/- 1 to 100 +/- 2 mmHg on day 1 and was 108 +/- 4 mmHg by day 7 of insulin. CO tended to decrease during insulin infusion, although not significantly, averaging 94 +/- 4% of the control value of 121 +/- 7 ml/min. Heart rate did not change significantly from the control value of 384 +/- 8 beats/min. TPR increased significantly to 122 +/- 11% of control by day 7. In five rats, glomerular filtration rate and effective renal plasma flow decreased to 73 +/- 4 and 66 +/- 5% of control, respectively, during insulin. Urinary sodium excretion averaged 2.6 +/- 0.1 and 2.7 +/- 0.1 meq/day during the control and insulin-infusion periods, respectively. These results indicate that insulin hypertension in rats is initiated by an increase in TPR rather than by increased CO. Also, the fact that sodium balance was maintained at elevated arterial pressure suggests that the ability of the kidneys to excrete sodium was impaired chronically during insulin infusion.

Animals↗

PubMed1982

Problems with plethysmographic estimation of lung volume in infants and young children.

In 57 infants and very young children, less than 2 yr of age and with a variety of cardiopulmonary illnesses, problems were encountered in the estimation of lung volume with the plethysmographic technique. In 19 subjects calculated thoracic gas volume (TGV) was found to be consistently larger when airway occlusions were performed at low lung volumes than when performed at higher lung volumes. In 13 infants, changes in intraesophageal pressure (Pes) during airway occlusions were found to be larger than simultaneous changes in mouth pressure. In 25 subjects in whom none of the above changes were observed, total pulmonary resistance (TPR) and airway resistance (Raw) did not differ significantly [mean TPR, 50.1 +/- 27.5 cmH2O X l-1; mean Raw, 48.1 +/- 26.5 (P greater than 0.5)]. In the 13 subjects in whom the delta Pes-to-delta Pm occlusion ratio exceeded 1.05, closest agreement with specific resistance (sRaw) and TPR derived lung volume was found when TGV was calculated with delta Pes rather than mouth pressure change (delta Pm). A similar close agreement with the sRaw TPR derived volume was obtained when TGV was calculated during airway occlusions at the higher lung volume. Two separate lung models are proposed to explain these observations, one with a segmental airway closure and the other with more a generalized airway closure. If plethysmographic techniques are to be used in these young subjects for the estimation of lung volume and airway resistance, possible errors may be reduced by performing airway occlusions at lung volumes above functional residual capacity and noting the delta Pes-to-delta Pm ratio obtained during the occlusion.

Airway Resistance↗

PubMed1997

Intracerebroventricular propranolol prevented vascular resistance increases on arousal from sleep apnea.

Despite the increased risk of sudden cardiac death associated with sleep apnea, little is known about mechanisms controlling cardiovascular responses to sleep apnea and arousal. Chronically instrumented pigs were used to investigate the effects of airway obstruction (AO) during rapid-eye-movement (REM) and non-REM (NREM) sleep and arousal on mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR). A stainless steel cannula was implanted in the lateral cerebral ventricle. During REM sleep, HR was 133 +/- 10 beats/min, MAP was 65 +/- 8 mmHg, CO was 1,435 +/- 69 ml/min, and TPR was 0.046 +/- 0.004 mmHg.ml-1.min. During AO, CO decreased by 90 +/- 17 ml/min (P < 0.05). On arousal from AO, MAP increased by 15 +/- 3 mmHg, HR increased by 10 +/- 3 beats/min, and TPR increased by 0.008 +/- 0.001 mmHg.ml-1.min (all P < 0.05). Changes during NREM were similar but were more modest during AO. After the intracerebroventricular administration of propranolol (50 micrograms/kg; a beta-adrenoreceptor blocking agent), decreases in CO during AO and increases in HR during arousal were intact, but increases in MAP and TPR were no longer significant. These data suggest that vascular responses to AO during sleep may be regulated in part by beta-adrenergic receptors in the central nervous system.

Adrenergic beta-Antagonists↗

PubMed1998

Percutaneous suprapubic transvesical route: a new and comfortable method of intraprostatic injection.

To assess the efficacy and safety of the percutaneous suprapubic transvesical route (STR) for intraprostatic antibiotic injections and compare it with the transperineal route (TPR), a total of 37 patients suffering from chronic bacterial prostatitis, resistant even to treatment with fluoroquinolones, were randomized to intraprostatic amikacin injections using either STR (n = 19) or TPR (n = 18). Follow-ups were done at weeks 4, 12, 24 and 52. Patients found to have failures at the first follow-up were given an additional injection using the initial route. At the 24th week, 15 patients from both groups were given another injection using the alternative route and were asked to report any subsequent voiding difficulties and compare the discomfort and pain experienced. At the end of 52 weeks, bacteriological cure rates did not differ significantly (44.4 vs. 47.3%). Overall improvement rates in the severity of symptoms and signs were similiar. Considerable difficulty in directing the needle to the prostate due to an excessive amount of subcutaneous fat was experienced, and more than 1 skin puncture was necessary in 5 of the STR group, whereas in the TPR group 7 patients with external hemorrhoids and 1 patient with a rectal fissure had prominent discomfort and pain during the transperineal procedures. Complications such as dysuria or hemospermia were encountered infrequently in both groups, but hematuria was observed more frequently in the STR group (85 vs. 54%). Less discomfort (p < 0.01) and pain (p < 0.01) were reported during access to the prostate by STR, but pain during the injection of the drug did not differ significantly. In conclusion, the percutaneous STR may well be used efficiently and comfortably as an alternative method to TPR when intraprostatic injections are needed in a limited number of cases such as those with a known hypersensitivity to fluoroquinolones or with a history of failure despite long-term systemic treatment with these agents.

Adult↗

PubMed2000

Peripheral vascular endothelial dysfunction and apoptosis in old monkeys.

To determine the effects of aging on vasoactivity in a primate model (Macaca fascicularis), 13 young male monkeys (aged 7.1+/-0.4 years) and 9 old male monkeys (aged 19.8+/-0.6 years) were chronically instrumented for measurement of left ventricular and aortic pressures and cardiac output. Total cholesterol, triglyceride, and fasting blood sugar levels were not different between the 2 groups. There were no significant differences in baseline mean aortic pressure and total peripheral resistance (TPR) in the young monkeys versus the old monkeys. TPR fell less (P<0.05) with acetylcholine (1 microg/kg) in old monkeys (-25+/-1%) than in young monkeys (-34+/-2%), whereas decreases in TPR with sodium nitroprusside were similar in old and young monkeys. There was no evidence of atherosclerosis, but apoptosis of endothelial cells was enhanced (P<0.05) in the aortas and femoral arteries, but not in the media, of the old monkeys. There was a relationship (r=0.62, P=0.013) between the incidence of terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)-positive endothelial cells and endothelial cell density in the femoral artery. The reduced endothelial cell density was also correlated (r=0.82, P<0.01) with depressed TPR responses to acetylcholine. Thus, vascular endothelial dysfunction was present in old monkeys without evidence of atherosclerosis, which may be due to endothelial apoptosis and reduced endothelial cell density.

Acetylcholine↗

PubMed2004

Vasoconstrictor reserve and sympathetic neural control of orthostasis.

BACKGROUND: We tested the hypothesis that individual variability in orthostatic tolerance is dependent on the degree of neural and vasomotor reserve available for vasoconstriction. METHODS AND RESULTS: Muscle sympathetic nerve activity (MSNA) and hemodynamics were measured in 12 healthy young volunteers during 60 degrees head-up tilt (HUT), followed by a cold pressor test (CPT) in HUT. Orthostatic tolerance was determined by progressive lower-body negative pressure (LBNP) to presyncope. The same protocols were performed randomly in normovolemic and hypovolemic conditions. We found that mean arterial pressure increased and stroke volume decreased, whereas heart rate (HR), MSNA, and total peripheral resistance (TPR) increased during HUT (all P<0.01). Application of the CPT in HUT did not increase HR or decrease stroke volume further but elevated mean arterial pressure (P<0.01) and increased MSNA and TPR in some subjects. There was a positive correlation between the time to presyncope from -50 mm Hg LBNP (equivalent to 60 degrees HUT alone) and the changes in MSNA produced by the CPT under both conditions (r=0.442, P=0.039). Those who had greater increases in MSNA had greater increases in TPR during the CPT and longer time to presyncope (both P<0.05). One subject had dramatic increases in MSNA but small increases in TPR during the CPT, which indicates a disassociation between sympathetic activity and the increase in peripheral vascular resistance. CONCLUSIONS: These results support our hypothesis and suggest that vasoconstrictor capability is a contributor to orthostatic tolerance in humans. Vasoconstrictor reserve therefore may be one mechanism underlying individual variability in orthostatic intolerance.

Adult↗

PubMedDate not supplied

Hemodynamic mechanisms of adaptation to chronic high sodium intake in normal humans.

The long-term hemodynamic effects of a high dietary sodium intake were studied in 10 young normal subjects. After a 4-day diet of 10mEq of sodium and 60 mEq of potassium per day the mean arterial blood pressure (MAP) was 82.3 +/- 15.1 mmHg, the cardiac index (CI) was 2.32 +/- 0.69 liter/min/m2, and total peripheral resistance (TPR) was 1778 +/- 947 dyne sec cm-5. After 4 to 6 days of 200 mEq of sodium and 60 mEq of potassium per day, MAP was 84.3 +/- 20.9 mm Hg, CI had risen to 2.53 +/- 0.61 liter/min/m2, and TPR fell to 1437 +/- 328 dyne sec cm-5. After 6 months of unrestricted sodium intake, urinary sodium excretion (UNa) was 144.1 +/- 51.9 mEq/24 hrs (p less than 0.001), MAP remained at 83.1 +/- 13.8 mm Hg, CI had risen to 3.11 +/- 1.01 liter/min/m2 (p less than 0.05) and TPR was 1268 +/- 444 dyne sec cm-5. After 12 months, UNa had risen to 171.5 +/- 97.6 mEq/24 hrs (p less than 0.005), while MAP remained at 82.4 +/- 17.9 mm Hg, CI at 3.08 +/- 1.16 liter/min/m2 (p less than 0.05), and TPR at 1282 +/- 500 dyne/sec/cm-5. Thus, cardiac index rises significantly with sodium intake in normal subjects and remains at a higher level for as long as 12 months. Blood pressure does not rise because TRP falls proportionately.

Adaptation, Physiological↗

PubMed1976

Changes in cardiac output and total peripheral resistance during development of renal hypertension in the rabbit: lack of confomity with the autoregulation theory.

Serial measurements of cardiac output (CO), mean arterial pressure (MAP), heart rate, and total peripheral resistance (TPR), were made on unanesthetized rabbits with previously implanted Doppler flowmeters. After 2 days of control measurements the rabbits were subjected alternatively to bilateral renal cellophane wrapping (wrap group) or to sham operation and additional measurements were made 1, 2, 4, 8, 16, 25, and 32 days after operation. During the 1st week after operation changes in CO were identical in the wrap and sham-operated groups, with an overall increase to a value of 110% of control on day 4 (P less than 0.05). Thereafter CO fell gradually, reaching 75% of control by day 32 in the wrap group, but only 95% of control in the sham-operated group. When CO was expressed per unit of body weight the latter differences were somewhat reduced, but still were significant. In wrap animals MAP and TPR rose progressively to 155% and 194% of control by day 32. In the sham-operated group the corresponding increases to 108% and 118% of control were significantly smaller. The MAP and TPR of the renal wrap rabbits exceeded the values in sham-operated rabbits, even over the 1st week after operation, by an average for MAP of 8.6 +/- 1.4% (P less than 0.001), and for TPR of 8.0 +/- 2.5% (P = 0.01). The results suggest that the changes in CO during the 1st week were a nonspecific consequence of the preceding wrap or sham operation. They bore no apparent relationship to the subsequent development of the hypertension which was "resistance-mediated" from the earliest stages. We conclude that the present findings for the rabbit differ from those reported for other species and do not conform to the changes predicted by the autoregulation theory of the pathogenesis of hypertension.

Animals↗

PubMed1976

Site of myocardial infarction. A determinant of the cardiovascular changes induced in the cat by coronary occlusion.

The influence of site of acute myocardial infarction on heart rate, blood pressure, cardiac output, total peripheral resistance (TPR), cardiac rhythm, and mortality was determined in 58 anesthetized cats by occlusion of either the left anterior descending (LAD), left circumflex or right coronary artery. LAD occlusion resulted in immediate decrease in cardiac output, heart rate, and blood pressure, an increase in TPR, and cardiac rhythm changes including premature ventricular beats, ventricular tachycardia, and occasionally ventricular fibrillation. The decrease in cardiac output and increase in TPR persisted in the cats surviving a ventricular arrhythmia. In contrast, right coronary occlusion resulted in a considerably smaller decrease in cardiac output. TPR did not increase, atrioventricular condition disturbances were common, and sinus bradycardia and hypotension persisted in the cats recovering from an arrhythmia. Left circumflex ligation resulted in cardiovascular changes intermediate between those produced by occlusion of the LAD or the right coronary artery. Mortality was similar in each of the three groups. We studied the coronary artery anatomy in 12 cats. In 10, the blood supply to the sinus node was from the right coronary artery and in 2, from the left circumflex coronary artery. The atrioventricular node artery arose from the right in 9 cats, and from the left circumflex in 3. The right coronary artery was dominant in 9 cats and the left in 3. In conclusion, the site of experimental coronary occlusion in cats is a major determinant of the hemodynamic and cardiac rhythm changes occurring after acute myocardial infarction. The cardiovascular responses evoked by ligation are related in part to the anatomical distribution of the occluded artery.

Animals↗

PubMed1993

Depressed beta-adrenergic receptor- and endothelium-mediated vasodilation in conscious dogs with heart failure.

Peripheral vasodilator responsiveness was examined in pacing-induced heart failure (HF) in 11 conscious dogs chronically instrumented for measurement of systemic (total peripheral resistance [TPR]) and local (iliac blood flow) vascular resistance. Dose responses to isoproterenol (ISO), acetylcholine (ACh), and nitroglycerin (NTG) were examined in the same dogs before pacing (control) and after 4 to 7 weeks of rapid ventricular pacing, which induced congestive HF, characterized by increased left ventricular end-diastolic pressure (6.7 +/- 0.4 [control] versus 28 +/- 1.5 [HF] mm Hg) and decreased cardiac output (-30 +/- 5%) and left ventricular dP/dt (-53 +/- 3%), as well as ascites and peripheral edema. In the control state, TPR fell by 57 +/- 2% in response to ISO (100 ng/kg), by 61 +/- 3% in response to ACh (3 micrograms/kg), and by 55 +/- 2% in response to NTG (10 micrograms/kg). In HF, smaller decreases (P < .05) in TPR were observed with the same doses of ISO (-50 +/- 2%) and ACh (-49 +/- 2%) but not with NTG (-58 +/- 3%). Depressed responses to systemic ISO and ACh, but not NTG, were observed in HF in the presence of ganglionic blockade and also after local administration of smaller doses of the drugs in the absence of ganglionic blockade, but where systemic effects were not elicited. Inhibition of nitric oxide synthase increased TPR to a greater degree before HF (+154 +/- 28% [control]) than after (+80 +/- 22% [HF]) and eliminated the depressed responses to ACh but not to ISO. beta-Adrenergic receptor density, as determined by 125I-cyanopindolol binding in membrane preparations from mesenteric vessels was significantly decreased after HF (130 +/- 3 [control] versus 100 +/- 8 [HF] fmol/mg, P < .05) without any change in affinity. Thus, peripheral vascular beta-adrenergic receptor downregulation occurs in HF, independent of altered endothelium-mediated peripheral vasodilation.

Acetylcholine↗

PubMed1989

Quantitative contribution of systemic vascular autoregulation in acute hypertension in conscious dogs.

Experiments were performed in nine conscious dogs to quantitate the contribution of systemic vascular autoregulation to the increases in total peripheral resistance (TPR) and mean arterial pressure (MAP) produced by angiotensin II (ANG II), arginine vasopressin (AVP), and norepinephrine (NE). We hypothesized that if autoregulatory vasoconstriction is significant, then the increase in TPR produced by vasoconstrictor infusion will be greater when MAP is controlled at hypertensive values than when the increase in pressure is prevented by controlling MAP at the animal's normotensive value. Each drug was infused at a dose sufficient to increase MAP by 50%. Then, a constant rate of vasoconstrictor infusion was maintained while MAP was controlled at hypertensive or normotensive levels for 15-min periods using a gravity reservoir connected to the left common carotid artery. During AVP infusion, TPR was significantly greater when MAP was controlled at hypertensive than at normotensive values. This autoregulatory-mediated vasoconstriction accounted for approximately three-fourths of the increase in MAP produced by AVP. No significant autoregulatory component was identified for the increases in TPR and MAP produced by ANG II or NE. We conclude that systemic vascular autoregulation is a powerful physiological property that contributes to the hemodynamic response to pressor doses of AVP.

Angiotensin II↗

PubMed2004

Differences in resting cardiovascular parameters in 10- to 15-year-old children of different ethnicity: the contribution of physiological and psychological factors.

BACKGROUND: The health status of children in the North West Province of South Africa was examined using the Transition and Health during Urbanization in South Africa in Children study. This is an epidemiological, cross-sectional study for which 1,244 children between 10 and 15 years of age were recruited from 44 schools. PURPOSE: Our objective was to investigate whether differences exist between resting cardiovascular parameters of Black, White, colored, and Indian children and evaluate the contribution of physiological and psychological factors. METHODS: Blood pressure was monitored with the Finapres apparatus. By means of the Fast Modelflo software program, the systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure, heart rate, cardiac output (CO), total peripheral resistance (TPR), and "Windkessel" compliance (Cw) of the arterial system were obtained. The psychological data were obtained by validated questionnaires. RESULTS: After correction for body mass index, the SBP of the White children was significantly higher (p < .05) than the SBP of the other ethnic groups. The DBP showed no significant differences. The TPR measurements of the Black and colored children were significantly higher (p < .05) than the TPR of the White children, and the Cw measurements of the Black and colored children were significantly lower than the Cw of the White children. Significant correlations (p < .05) were found between the SV, CO, TPR, Cw, and the total score on violence in the Black and colored children. CONCLUSIONS: There are differences in the resting cardiovascular parameters in the different ethnic groups studied. The higher levels of violence to which the Black and colored children are exposed could alter vascular sensitivity to sympathetic stimulation. This may contribute via the higher -adrenergic sensitivity to the pathogenesis of hypertension in their later lives.

Adolescent↗

PubMed2005

Structure-function analysis of squirrel monkey FK506-binding protein 51, a potent inhibitor of glucocorticoid receptor activity.

FK506-binding protein 51 (FKBP51) and FKBP52 are large molecular weight immunophilins that are part of the mature glucocorticoid receptor (GR) heterocomplex. These proteins possess peptidyl-prolyl isomerase (PPIase) and tetratricopeptide repeats (TPR) domains that are important for modulation of GR activity. A naturally occurring animal model of glucocorticoid resistance, the squirrel monkey, results from the relative overexpression of FKBP51 that renders the GR in a low-affinity state. In vitro studies demonstrated that the squirrel monkey form of FKBP51 is greater than 6-fold more potent than human FKBP51 in this respect. The goals of these studies were to determine the roles of the TPR and PPIase domains in the inhibitory activity of squirrel monkey FKBP51 and to gain insight into structural features of squirrel monkey FKBP51 responsible for potent inhibition of dexamethasone-stimulated GR activity. Mutations in the TPR of squirrel monkey FKBP51 that inhibit association with heat shock protein 90 blocked GR inhibitory activity. Mutations that abrogate the PPIase activity of squirrel monkey FKBP51 had no effect on GR inhibitory activity. Chimeras of squirrel monkey and human FKBP51 were tested to identify domains responsible for their different inhibitory potencies. Amino acid differences in domains FK1 and FK2 between squirrel monkey and human FKBP51 contribute equally to the enhanced inhibitory activity of squirrel monkey FKBP51. Furthermore, squirrel monkey FKBP51 in which either FK1 or FK2 was deleted lacked GR inhibitory activity. Thus, the potent inhibitory activity of squirrel monkey FKBP51 involves both FK domains and the heat shock protein 90-binding TPR domain.

Animals↗

PubMed1983

The hemodynamics in young patients with borderline hypertension.

Hemodynamics in supine position were studied echocardiographically in 56 young patients with borderline hypertension and 56 age-matched normotensive subjects. In hypertensive patients, the cardiac index (CI) did not increase, but the total peripheral resistance (TPR) increased significantly (p less than 0.005). The hypertensive patients were classified into 2 groups, according to the level of the CI. In patients in group A ("normal" CI), the CI, heart rate and the mean circumferential fiber shortening velocity (mVCF) were normal, but the TPR was increased significantly. In patients in group B ("high" CI), the CI, heart rate and the mVCF increased significantly (hyperkinetic state), but the TPR was normal. Plasma renin activity (PRA) was significantly higher in patients in group B than the normal subjects, but the level of PRA in patients in group A was normal. These findings support the hypothesis that sympathetic nervous activity increases in patients in group B, but not in those in group A. Therefore, this study provides evidence that the TPR is abnormal in patients with borderline hypertension, and an impaired neurogenic activity seems to be important in the early stage of hypertension, as in borderline hypertension associated with a hyperkinetic circulatory state (group B).

Adult↗

PubMed1992

Differing actions of endothelin-1 on canine systemic resistance and capacitance vessels.

In anesthetized open-chest dogs, an intravenous bolus injection of endothelin-1 (ET-1, 400 pmol/kg) caused transient hypotension (initial hypotensive phase; phase 1), followed by a continuous elevation of blood pressure (late hypertensive phase; phase 2). The constriction and dilation of the systemic capacitance and resistance vessels were evaluated from the change in mean circulatory pressure (MCP) and in total peripheral resistance (TPR) in phases 1 and 2. To examine the modification of the action of ET-1 on the blood vessels by the baroceptor reflex or by the endothelium-derived relaxing factor (EDRF) released by ET-1 in phase 1, we performed experiments in dogs under total spinal anesthesia (TSA group), methylene blue-treated dogs (MB group) as well as in the untreated dogs (control group). ET-1 decreased the TPR significantly, and increased the MCP significantly in phase 1 in the control (n = 8) and TSA (n = 8) groups; there was no difference between the groups. ET-1 had no significant effect on TPR but increased the MCP significantly in MB group (n = 8) during phase 1. The percentage increase of MCP in the MB group significantly exceeded that of the control group. ET-1 increased both the TPR and MCP significantly in phase 2 in the control group (n = 8). This study indicated that the vasoconstrictor action of ET-1 on the systemic capacitance vessels in phase 1 did not result from a baroceptor reflex, and that the vasodilator action of ET-1 on the systemic resistance vessels may be at least in part mediated via EDRF released by ET-1. We suggest that the vasoconstrictor action of ET-1 on the systemic capacitance vessels is strong, but the vasodilator action of EDRF on the systemic capacitance vessels is weak.

Animals↗

PubMed1985

Venodilating action of nipradilol (K-351) in the pithed rat pretreated with dihydroergotamine.

The venodilating action of nipradilol was investigated by monitoring arterial blood pressure (BP), cardiac output (CO), heart rate (HR) and central venous pressure (CVP) in pithed rats treated with dihydroergotamine (DHE). DHE increased CVP and produced a simultaneous rise in BP and CO without appreciable changes in total peripheral resistance (TPR) and HR, indicating that DHE reduces venous capacity through venoconstriction. Nipradilol caused a fall in CVP, BP and CO without changing the TPR in the DHE-pretreated rat. By comparison, hydralazine reduced BP and TPR without changes in CO. Propranolol produced only a transient decrease in BP and TPR. These results indicate that nipradilol dilates venous capacitance vessels and thereby decreases cardiac filling pressure in animals with high venous tone, whereas hydralazine preferentially dilates resistance vessels.

Adrenergic alpha-Antagonists↗

PubMed1986

Assessment of the cardiohemodynamic effects of ibopamine, an orally-active dopamine analogue, in the anesthetized open-chest guinea pig and the isolated guinea pig atria.

In the anesthetized open-chest guinea pig, ibopamine (10-300 micrograms/kg, i.v.), epinine (10-100 micrograms/kg, i.v.) and dopamine (10-300 micrograms/kg, i.v.) produced dose-related increases in heart rate (prevented by 20 micrograms/kg pindolol, i.v.), left ventricular dP/dt max and aortic flow. Ibopamine produced pressor effects (prevented by 0.5 mg/kg phentolamine, i.v.), while dopamine produced a slight depressor effect. A biphasic response (the pressor phase followed by a depressor) was observed after epinine, although the depressor phase was not significant. Calculated total peripheral resistance (TPR) tended to be increased after ibopamine and epinine (initial phase), while it was decreased after dopamine. Pindolol potentiated the increase in TPR produced by ibopamine and epinine, while the increase in TPR was converted to the decrease after phentolamine. Decreases in TPR produced by epinine and the highest dose of dopamine were inhibited by pindolol. In the isolated guinea pig atria, ibopamine (10(-6)-10(-4) M) increased the atrial rate and the developed tension in a concentration-related manner. The positive chronotropic and inotropic effects of ibopamine were of the same order as those of epinine.

Animals↗