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PubMed1996

[Effects of efonidipine hydrochloride, a calcium antagonist derived from dihydropyridine, on acute myocardial ischemia in anesthetized open-chest dogs].

Effects of efonidipine hydrochloride (NZ-105), a dihydropyridine calcium antagonist, on the cardiovascular system were studied in dogs, in which the left anterior descending coronary artery (LAD) was ligated for 50 min. NZ-105 (10 or 30 micrograms/kg), nifedipine (NIF, 1 or 3 micrograms/kg) or nisoldipine (NIS, 1 or 3 micrograms/kg) was injected i.v. before LAD ligation. NZ-105, NIS or NIF decreased the total peripheral resistance (TPR) and blood pressure (BP) and increased the cardiac output (CO) and regional myocardial blood flow (RBF) dose-dependently. LAD ligation decreased RBF and produced segmental bulging in the ischemic area, decreased BP and CO, and did not change TPR. NZ-105, NIF or NIS attenuated the LAD ligation-induced regional myocardial changes. During LAD ligation, in the presence of NZ-105 (30 micrograms/kg), the values of heart rate (HR), BP, and TPR were lower, and that of CO was higher than those in the absence of the drug. Similar results were obtained with NIS (3 micrograms/kg) except that the value of HR in the presence of NIS was not lower. During ischemia, the presence of NIF (3 micrograms/kg), did not significantly change the values of the systemic circulation from those observed in the absence of NIF. In conclusion, NZ-105 may exert a cardioprotective effect by decreasing the oxygen demand of the ischemic heart.

Animals↗

PubMed1985

[Effects of isosorbide 5-mononitrate on cardiovascular function. (II). Effects on pre-load and after-load].

Effects of isosorbide 5-mononitrate (5-ISMN) on cardiovascular function were compared with those of verapamil hydrochloride and propranolol hydrochloride in anesthetized open-chest dogs. Intravenous injection of 5-ISMN (3 mg/kg) considerably lowered systolic blood pressure (SBP). Especially, stroke volume (SV), cardiac output (CO), cardiac work (CW) and systolic right ventricular pressure (SRVP) were significantly decreased. 5-ISMN also produced a continuous reduction in mean pulmonary artery pressure (MPAP), mean pulmonary capillary wedge pressure (MPCWP) and mean right atrium pressure (MRAP), while heart rate (HR) and total peripheral resistance (TPR) were not altered significantly. Intravenous injection of verapamil (0.3 mg/kg) considerably lowered diastolic blood pressure (DBP). Verapamil also caused a significant decrease in HR, CW and TPR and a slight decrease in SRVP and MPCWP. However, SV was significantly increased, and slight increases in MPAP and MRAP were also observed. Propranolol (0.5 mg/kg, i.v.) greatly decreased HR together with CO, CW, SRVP and MPAP and slightly decreased MPCWP, while it caused a considerable increase in 3V and a slight increase in TPR. The finding that administration of 5-ISMN resulted in reduction of pre-load and after-load suggests the possibility that this drug might decrease venous return and thereby reduce myocardial oxygen requirements.

Animals↗

PubMed2003

Randomized controlled trial of a computer-assisted learning program to improve caries detection from bitewing radiographs.

OBJECTIVES: To investigate whether using a computer-assisted learning (CAL) calibration program improves the accuracy of dental students in caries detection from bitewing radiographs. METHODS: Dental students were assigned to an experimental (n=33) and control (n=34) group using a randomized block design. The experimental group used the CAL program with feedback to calibrate themselves against experts in radiographic caries detection and a histological gold standard of the actual clinical condition. Feedback was provided visually of the actual tooth surface condition and in the form of graphics showing diagnostic accuracy performance measures. Performance was tested before the program (for the control group) and after the program (for the experimental group) by assessing surfaces (n=56) from a new independent digital test set of evaluation radiographs for the presence, histologically, of dentine caries (n=23). The summary receiver operating characteristic (SROC) method for summarizing true positive ratio (TPR) (sensitivity) and false positive ratio (FPR) (1-specificity) was used to analyse the dichotomous data. Differences between the control and experimental groups were tested for (a) the area under the SROC curve (A(z)) and (b) the TPR, FPR and diagnostic odds ratio (DOR) using the Mann-Whitney test (P<0.05). RESULTS: The mean TPR for dentine caries detection was 76.3% (SD 13.0%) for the experimental group and 66.9% (SD 14.8%) for the control group (P=0.005). Mean FPRs were similar (experimental 28.1% and control 28.7%; P>0.5). The area under the SROC curve A(z) was 0.832 for the experimental group and 0.773 for the control group (P=0.002). The mean DOR for dentine caries in the experimental group (12.4) was better than that in the control group (8.8) (P=0.003). CONCLUSIONS: The CAL program does improve diagnostic performance. Improving the cognitive feedback provided by the program should be considered before implementation.

Area Under Curve↗

PubMed1997

The value of emergency CT studies in spontaneous rupture of hepatocellular carcinoma. Analysis for tumor protrusion and hemorrhagic ascites.

CT characteristics of spontaneous rupture of HCC (n = 13) were reviewed retrospectively, and the value of emergency CT studies in this disease was evaluated. Especially, tumor protrusion ratio (TPR) and ascitic CT numbers were measured to for comparison with the data for unruptured HCCs and ordinary (e.g. non hemorrhagic) ascites (n = 13). As a result, except for diffuse type HCCs, the TPR was significantly higher than for the unruptured HCCs. Nine cases had intraperitoneal HDAs, and the laterality of the HDAs corresponded with that of the ruptured tumors in 8 cases. Also, the ascitic CT numbers apart from the HDA were still higher than the ordinary ascites. Therefore, a high TPR, HDAs adjacent to the tumor, and elevated ascitic CT numbers are important CT manifestations indicating HCC rupture. Diffuse HCCs, however, require careful clinical evaluation.

Adult↗

PubMed2001

Role of nitric oxide in regional blood flow in angiotensin II-induced hypertensive rats.

The present study was designed to evaluate the contribution of nitric oxide (NO) to regional hemodynamics during the early phase of angiotensin II (Ang II)-induced hypertension. The responses of regional blood flow to chronic NO synthase inhibition with N(G)-nitro-L-arginine methyl ester (L-NAME) were assessed using radioactive microspheres in conscious Ang II-infused hypertensive rats. Ang II-infused rats (270 ng/kg/min, subcutaneously for 12 days: n=11) showed higher mean arterial pressure (MAP: 153+/-4 mmHg) and total peripheral resistance (TPR: 1.61+/-0.06 mmHg/min/ml), and lower cardiac output (CO: 102+/-3 ml/min) than vehicle-infused normotensive rats (115+/-2 mmHg, 0.96+/-0.05 mmHg/min/ml and 130+/-7 ml/min, n=11, respectively). The blood flow rates in the brain, spleen, large intestine and skin were significantly reduced in Ang III-infused rats compared with vehicle-infused rats, while those in the lung, heart, liver, kidney, adrenal gland, small intestine, and skeletal muscle were similar. Treating Ang II-infused rats with L-NAME (75 mg/l in drinking water for 10 days, n=11) resulted in higher MAP (166+/-6 mmHg) and TPR (1.89+/-0.18 mmHg/min/ml) and lower CO (87+/-7 m/min) than untreated Ang II-infused rats. L-NAME-treated Ang II-infused rats showed widespread increases in regional vascular resistance and reduced blood flow rates in the kidney (3.81+/-0.27 ml/min/g) and skeletal muscle (0.20+/-0.03 ml/min/g) compared with untreated Ang II-infused rats (6.88+/-0.27 and 0.33+/-0.04 ml/min/g, respectively). However, there were no significant differences in the flow rates of other organs investigated between these animals. An NO donor, (+/-)-(E)-4-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexenamide (FK409: 30 microg/kg/min, i.v.), significantly decreased MAP (110+/-6 mmHg) and TPR (1.23+/-0.18 mmHg/min/ml) without significant changes in CO (89+/-9 ml/min) in L-NAME-treated Ang II-infused rats. Furthermore, FK409 partially reversed blood flow rates in the kidney (4.72+/-0.40 ml/min/g) and skeletal muscle (0.25+/-0.02 ml/min/g)in these animals. These results suggest that NO counteracts, at least in part, the vasoconstrictor effects of elevated Ang II levels in renal and skeletal muscle vascular beds, and is an important modulator in the regulation of blood flow to these organs during the development of Ang II-induced hypertension.

Angiotensin II↗

PubMed1996

Lisinopril attenuates acute hypoxic pulmonary vasoconstriction in humans.

OBJECTIVE: We have studied the effects of angiotensin-converting enzyme (ACE) inhibition with lisinopril on acute hypoxic pulmonary vasoconstriction (HPV). DESIGN: Randomized, double-blind, placebo-controlled study in ten healthy volunteers. Subjects received four daily doses of lisinopril or matched placebo before attending the laboratory 5 h after taking the final dose. After reaching a resting hemodynamic state, subjects were made hypoxemic (SaO2, 75 to 80%) for 30 min. MEASUREMENTS: Pulmonary and systemic hemodynamic parameters were measured noninvasively at baseline and after 30 min of hypoxemia. RESULTS: Mean pulmonary artery pressure (MPAP) and total pulmonary vascular resistance (TPR) were similar at baseline on both study days. The increase in MPAP induced by hypoxemia was significantly blunted by pretreatment with lisinopril (means and 95% confidence interval [CI] for difference) 13.4 mm Hg vs placebo 19.6 mm Hg (95% CI, 2.5, 9.9). Likewise, the TPR response to hypoxemia was significantly blunted by lisinopril: 124 dyne.s.cm-5 vs placebo 179 dyne.s.cm-5 (95% CI, 11, 99). Lisinopril had no confounding systemic effects on mean arterial pressure, cardiac output, or systemic vascular resistance at baseline or in response to hypoxemia. CONCLUSIONS: Lisinopril therefore significantly attenuated the pulmonary pressor response to hypoxemia without decreasing baseline MPAP or TPR. This suggests that angiotensin II might play a modulatory role during HPV in man and that ACE inhibition may be a useful adjunctive treatment in hypoxemic pulmonary hypertension.

Adult↗

PubMed1996

Angiotensin II receptor blockade and effects on pulmonary hemodynamics and hypoxic pulmonary vasoconstriction in humans.

STUDY OBJECTIVE: We examined the hypothesis that angiotensin II (ANG II) is a modulator of pulmonary vascular tone by examining the effects of ANG II blockade on pulmonary hemodynamics during normoxemia and hypoxemia in normal volunteers with an activated renin angiotensin system (RAS). PARTICIPANTS AND INTERVENTIONS: Eight normal volunteers, pretreated with furosemide, were studied on two separate occasions and received either an infusion of saralasin, 5 micrograms/kg/min, or placebo. After 20 min, they were rendered hypoxemic, by breathing N2/O2 mixture for 20 min to achieve arterial oxygen saturation (SaO2) of 85 to 90% adjusted for a further 20 min to achieve SaO2 of 75 to 80%. Doppler echocardiography was used to measure mean pulmonary artery pressure (MPAP), cardiac output, and hence total pulmonary vascular resistance (TPR). RESULTS: Saralasin compared with placebo resulted in a significant (p < 0.05) reduction in MPAP during normoxemia, 6.70 +/- 1.0 vs 11.7 +/- 1.3 mm Hg; at SaO2 of 85 to 90%, 14.7 +/- 1.4 vs 20.5 +/- 1.0 mm Hg; and at SaO2 of 75 to 80%, 18.1 +/- 1.9 vs 27.8 +/- 1.9 mm Hg, respectively. Likewise saralasin compared with placebo resulted in a significant reduction in TPR during normoxemia, 104 +/- 14 vs 180 +/- 20 dyne.s.cm-5; at SaO2 of 85 to 90%, 222 +/- 24 vs 295 +/- 21 dyne.s.cm-5; and at SaO2 of 75 to 80%, 238 +/- 21 vs 362 +/- 11 dyne.s.cm-5, respectively. The delta MPAP response to hypoxemia was likewise significantly (p < 0.01) attenuated by saralasin infusion compared with placebo: mean difference 5.0 mm Hg, 95% confidence interval (CI) 1.9 to 8.08, and there was a trend toward attenuation of the delta TPR response to hypoxemia (0.05 < p < 0.10): mean difference 47 dyne.s.cm-5, 95% CI, -10 to 105. CONCLUSION: In addition to causing pulmonary vasodilatation in the presence of an activated RAS, our results suggest that ANG II receptor blockade attenuates acute hypoxic pulmonary vasoconstriction and that ANG II may play a role in modulating this response in normal man.

Adult↗

PubMed2005

C-terminus of heat shock protein 70-interacting protein facilitates degradation of apoptosis signal-regulating kinase 1 and inhibits apoptosis signal-regulating kinase 1-dependent apoptosis.

Apoptosis signal-regulating kinase 1 (ASK1) is a mitogen-activated protein kinase kinase kinase (MAPKKK) that is regulated under conditions of cellular stress. ASK1 phosphorylates c-Jun N-terminal kinase (JNK) and elicits an apoptotic response. ASK1 activity is regulated at multiple levels, 1 of which is through inhibition by cytosolic chaperones of the heat shock protein (Hsp) 70 family. Among the proteins that determine Hsp70 function, CHIP (C-terminus of Hsp70-interacting protein) is a cochaperone and ubiquitin ligase that interacts with Hsp70 through an amino-terminal tetratricopeptide repeat (TPR) domain. Prominent among the cellular functions mediated by CHIP is protection against physiologic stress. Because ASK1 is known to contain a TPR-acceptor site, we examined the role of CHIP in regulating ASK1 function. CHIP interacted with ASK1 in a TPR-dependent fashion and induced ubiquitylation and proteasome-dependent degradation of ASK1. Targeting of ASK1 by CHIP inhibited JNK activation in response to oxidative challenge and reduced ASK1-dependent apoptosis, whereas short interfering RNA (siRNA)-dependent depletion of CHIP enhanced JNK activation. Consistent with its ability to reduce cytoplasmic ASK1 levels, CHIP triggered the translocation of ASK1 partner protein death-associated protein (Daxx) into the nucleus, where it is known to activate an antiapoptotic response. These results indicate that CHIP regulates ASK1 activity by inducing its ubiquitylation and degradation, which, together with its effects on Daxx localization, provides a mechanism for the antiapoptotic effects of CHIP observed in the face of cellular and physiologic stress.

Animals↗

PubMed1980

[Studies on the blood pressure control mechanism in essential hypertension: the relation of plasma norepinephrine concentrations to plasma renin activity and haemodynamics (author's transl)].

To elucidate the mechanism of blood pressure control in essential hypertension (EH), plasma norepinephrine concentrations (PNE), plasma renin activity (PRA), cardiac index (CI) and total peripheral resistance (TPR) were determined in normal subjects and those suffering from EH while resting and after standing with furosemide. The results were as follows: 1) PNE were 204 +/- 100 pg/ml (mean +/- S.D.) in normal subjects and 313 +/- 257 pg/ml in EH. PNE in EH were not significantly greater than in normal subjects, but in some patients with EH, PNE were above normal. 2) In both normal subjects and those suffering from EH, PNE and PRA showed a positive correlation (r = 0.45, p less than 0.05; r = 0.52, p less than 0.001; respectively). 3) In low renin EH, the response of PNE to the stimulation of standing with furosemide was significantly greater than in normal renin EH (p less than 0.05). 4) PNE in EH were independent of both TPR and CI. 5) There was a positive relation between PRA and CI (r = 0.44, p less than 0.05), and a slight negative relation between PRA and TPR (r = 0.36, 0.05 less than p less than 0.1). These results suggest that sympathetic nervous hypertonicity may be responsible for the activation of the renin-angiotensin system and that the interaction of both the sympathetic nervous system and the renin-angiotensin system may play an important role in the elevation of blood pressure. In low renin EH, the response of PNE to the stimulation of standing with furosemide may be normal and blood pressure may be controlled by both the sympathetic nervous system and the renin-angiotensin system.

Blood Pressure↗

PubMed2005

Effect of mutation of the tetratricopeptide repeat and asparatate-proline 2 domains of Sti1 on Hsp90 signaling and interaction in Saccharomyces cerevisiae.

Through simultaneous interactions with Hsp70 and Hsp90 via separate tetratricopeptide repeat (TPR) domains, the cochaperone protein Hop/Sti1 has been proposed to play a critical role in the transfer of client proteins from Hsp70 to Hsp90. However, no prior mutational analysis demonstrating a critical in vivo role for the TPR domains of Sti1 has been reported. We used site-directed mutagenesis of the TPR domains combined with a genetic screen to isolate mutations that disrupt Sti1 function. A single amino acid alteration in TPR2A disrupted Hsp90 interaction in vivo but did not significantly affect function. However, deletion of a conserved residue in TPR2A or mutations in the carboxy-terminal DP2 domain completely disrupted Sti1 function. Surprisingly, mutations in TPR1, previously shown to interact with Hsp70, were not sufficient to disrupt in vivo functions unless combined with mutations in TPR2B, suggesting that TPR1 and TPR2B have redundant or overlapping in vivo functions. We further examined the genetic and physical interaction of Sti1 with a mutant form of Hsp90, providing insight into the importance of the TPR2A domain of Sti1 in regulating Hsp90 function.

Amino Acid Substitution↗

PubMed1990

Fully automatic, noninvasive measurement of cardiac output by means of the CO2 rebreathing method and its clinical application to hypertensive patients.

A new device (called a hemodynamometer) employing the principle of the CO2 rebreathing method has been developed for the noninvasive automatic measurement of pulmonary blood flow (cardiac output = CO). The device can also measure oxygen consumption (VO2) and indirect blood pressure and record electrocardiographs (heart rate) at the same time and can automatically calculate total peripheral vascular resistance (TPR) by means of a computer. In this study, the hemodynamometer was used in 28 normotensive subjects and 42 patients with essential hypertension (27 with WHO stage I and 15 with WHO stage II) to evaluate hemodynamics during rest or ergometer exercise. To evaluate accuracy, the dye-dilution (cuvette) method was simultaneously employed in some subjects. The correlation coefficient (r) between CO measured by means of the hemodynamometer and CO measured by the cuvette method was 0.96 (n = 39) with a differential of 0.08 +/- 0.53 l/min and reproducibility was good (r = 0.88, n = 70). The average CO index for normotensive subjects at rest was 3.22 +/- 0.37 l/min/m2 (VO2 = 210 +/- 30 ml/min/m2) and agreed with previously reported values. A significant difference was observed between the hemodynamics (CO and TPR indices) of the WHO-I group and those of the WHO-II group during rest or mild exercise (25-watt load). Because it can measure CO and TPR easily and noninvasively, the hemodynamometer is considered useful for evaluating hemodynamic changes in hypertensive patients.

Adult↗

PubMed1992

Effects of denopamine with or without diltiazem on the ischemic heart of anesthetized dogs.

Effects of denopamine with or without diltiazem on the ischemic heart were investigated in anesthetized open-chest dogs. Partial occlusion of the left circumflex coronary artery (LCX) produced significant decreases in LCX flow and regional myocardial segment shortening rate (%SS) in the LCX-perfused area, and a significant increase in left ventricular enddiastolic pressure (LVEDP). Heart rate (HR) and mean aortic pressure (mAoP) were not altered, but aortic flow (AoF), positive first derivative of left ventricular pressure ((+)LVdP/dt), stroke volume (SV), stroke work index (SWI) and double product showed a tendency to decrease. Total peripheral vascular resistance (TPR) tended to increase. During coronary stenosis, saline infusion (vehicle group) did not change any parameter, but diltiazem infusion (diltiazem group) decreased HR, mAoP, TPR and double product and increased SV and SWI. Under these conditions, denopamine infusion produced increases in HR, mAoP, AoF, (+)LVdP/dt and double product and decreases in LVEDP and TPR in both groups. %SS in the left anterior descending coronary artery-perfused area was increased, but %SS in the LCX-perfused area was slightly decreased in both groups. SV and SWI were decreased by denopamine infusion in the vehicle group, while they were increased in the diltiazem group. Differences in changes in SV and SWI between the groups were statistically significant. Results suggest that combined treatment of denopamine and diltiazem may exert an advantage in alleviation of heart failure due to coronary stenosis.

Adrenergic beta-Agonists↗

PubMed1991

Effect of vasopressin on cardiovascular and renal functions and ANP release under plasma volume expansion.

To assess the mechanisms whereby arginine vasopressin (AVP) increases atrial natriuretic peptide (ANP) release and to examine whether AVP-mediated ANP release affects the effect of AVP on the cardiovascular and renal function, AVP was infused continuously at a rate of 20 ng.kg-1.min-1 for 75 min following 200 ng/kg bolus injection under stepwise increases in plasma volume in anesthetized dogs. Moreover, the effect of an AVP antagonist, a V1 blocker, 1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid)-2-(o-methyl)tyrosine AVP (TMeAVP), on these parameters was also investigated. In the control study, saline alone was infused. AVP infusion increased total peripheral resistance (TPR), pulmonary capillary wedge pressure (PCWP), and plasma ANP, but decreased cardiac index (CI) and heart rate (HR) without increases in mean arterial blood pressure (MABP). Stepwise rises in plasma volume further increased plasma ANP, CVP, CI and PCWP, but gradually decreased TPR. TMeAVP curtailed AVP-induced increases in TPR and plasma ANP as well as decreases in CI and HR. The replacement of ANP to prevent a fall in plasma ANP following TMeAVP never affected cardiovascular function. AVP infusion increased plasma volume accompanied by a fall in urinary Na excretion (UNaV) and urine flow (UF) under the stepwise plasma volume expansion compared to the control group, but did not affect mean circulatory filling pressure (MCFP). ANP administration enhanced UNaV and UF and decreased MCFP. These results indicate that AVP may preferentially increases ANP release via the increased cardiac afterload, not preload, but increased plasma ANP per se may not be involved directly in the AVP-induced cardiac suppression.

Animals↗

PubMed2000

Different patterns of DNA fragmentation and degradation of nuclear matrix proteins during apoptosis induced by radiation, hyperthermia or etoposide.

Several nuclear matrix proteins are substrates for proteolytic cleavage during apoptosis. Using Western blotting, the temporal patterns of cleavage of three nuclear matrix proteins (lamin B, NUMA and the nucleoporin TPR) were compared in HL60 cells induced to undergo apoptosis after irradiation, heat shock or treatment with etoposide. Flow cytometry was used to compare the kinetics of post-cleavage degradation of lamin B, NUMA and TPR after irradiation, and to correlate DNA fragmentation with protein degradation in cells induced to undergo apoptosis with different agents. During radiation-induced apoptosis, cleavage and subsequent degradation of lamin B, NUMA and TPR occurred with different kinetics. Low-molecular-weight DNA fragmentation occurred subsequent to the initiation of NUMA cleavage, coincided with lamin B cleavage, but occurred before more extensive degradation of lamin B and NUMA. A similar sequence was observed for cells treated with etoposide. However, during heat-induced apoptosis, cleavage of lamin B and NUMA occurred much sooner compared to other agents, with NUMA cleaved into multiple fragments within 15 min after heating. We conclude that the hierarchical sequence and kinetics of degradative events contributing to nuclear disassembly during apoptosis are highly dependent on the inducing agent. Furthermore, the nuclear pore complex, like the nuclear lamina and internal nuclear matrix, is a target for proteolytic cleavage.

Antigens, Nuclear↗

PubMed1976

Action of propranolol on arterial pressure and on cardiovascular reflexes.

In the rabbit, administration of 500 mug (+/-) propranolol into the lateral cerebral ventricle resulted in rapid leakage of drug into the blood. The drug produced a small reduction in blood pressure at 2 and 4 hours after injection but because of the rapid leakage, this could have been due to its peripheral actions. To investigate possible central mechanisms of action which were independent of peripheral effects, we tested the action of intravenously administered propranolol on the reflex rise in TPR evoked in rabbits by graded Valsalva-like manoeuvres. This was performed in unanaesthetised rabbits with Doppler flowmeters for measuring cardiac output. Graded expiratory pressures (EP) were applied to the inlet and outlet tubes of the tracheotomised animal's respiratory valve and to the cuff around their thorax and abdomen. Administration of propranolol at two levels (168 +/- 35 ng/ml, and 240 +/- 33 ng/ml) for 1 hour had no effect on slope and threshold of the EP-TPR relationship. By contrast to the minimal effects on the reflex with propranolol, the EP-related rise in TPR was attenuated by clonidine. We conclude that propranolol does not lower blood pressure in the rabbit by attenuating sympathetic constrictor activity.

Animals↗

PubMed1983

Increased systemic vascular responsiveness to catecholamines in spontaneously hypertensive rats.

Systemic vascular responsiveness to i.v. bolus injections of norepinephrine and tyramine was evaluated in adult male spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Changes in total peripheral resistance (TPR) were used as an index of vascular response. Dose-response curves were plotted with 1n-dose on the x-axis and percent of maximum change in TPR on the y-axis, and the following indices of responsiveness were used: slope, 1nED50, 1nx-intercept, and maximum response. Measurements were made before and after ganglionic blockade with pentolinium (5 mg/kg, i.v.). Cardiac output for TPR calculations was obtained from an implanted flow probe on the ascending aorta. The slopes and maximum responses to norepinephrine and tyramine were greater in SHR v. WKY, P less than .05, before and after pentolinium treatment. There were no significant differences in 1nED50 or 1nx-intercept between WKY and SHR for tyramine and norepinephrine prior to pentolinium. After pentolinium 1nED50 and 1nx-intercept were similar for SHR and WKY for norepinephrine, but were greater in SHR for tyramine. The results demonstrate an increased systemic vascular responsiveness to catecholamines in adult SHR, with no evidence of increased systemic vascular sensitivity. These findings are consistent with the concept of increased systemic vascular responsiveness to catecholamines in adult SHR secondary to structural changes in blood vessels.

Angiotensin II↗

PubMed1986

The role of the sympathetic nervous system in 2-kidney DOCA-hypertensive Yucatan miniature swine.

To assess the mechanism responsible for maintaining the elevated arterial pressure in 2-kidney DOCA treated Yucatan miniature swine, cardiovascular parameters and the responses to hexamethonium bromide (HMB) were evaluated in normal and DOCA treated animals. Using chronically instrumented conscious animals, measurements of mean arterial pressure (MAP), cardiac output (CO), and calculated total peripheral resistance (TPR) revealed that with DOCA hypertension MAP was increased 50-60 mmHg above controls. This increased pressure was due to an increase in TPR with CO remaining normal. HMB normalized the MAP of the DOCA animals via a selective lowering of TPR to a value similar to that of the controls. In DOCA hypertensive animals these functional changes, due to increased peripheral sympathetic nerve activity, were reflected by significantly elevated plasma norepinephrine. In this animal DOCA administration produces a neurogenic form of hypertension which appears to be analogous to essential hypertension in man.

Animals↗

PubMed1989

Hyperkinetic hemodynamic pattern in some borderline hypertension: differential responses to alpha and beta agonists.

Twenty eight male borderline hypertensive patients(BH), mean age of 19.72 +/- 2.80 years, were studied and matched with 28 normal controls (NC). Alpha-adrenergic responsiveness was estimated with DPD15 (the dosage of neosynephrine required for an increase of diastolic pressure of 15mmHg); beta-adrenergic responsiveness with CD25 (the dosage of isoproterenol required for an increase of heart rate of 25 beats/minute). Using CD25 of 1.0ug (mean of the NC), the BH could be subdivided into two specific types: 13 patients (46%) whose CD25 less than 1.0 ug, 0.50 +/- 0.24 (m +/- SD) had a hyperkinetic pattern; the remaining 15 patients (54%) whose CD25 greater than 1.0ug, 1.76 +/- 0.32 (m +/- SD), had a normokinetic one. Values of DPD15 of the two types were comparable. Cardiac index (CI, L/min/M2) and total peripheral resistance (TPR, dynes/sec/cm-5) of the two types manifested significant differences, both p less than 0.001. When plotting CI and TPR versus CD25, good correlations were obtained. In the BH group, the coefficient r was -0.73 between CI and CD25, + 0.70 between TPR and CD25; correlations were poor when plotting versus DPD15. Similar correlations also happened in the NC. The present study suggests that coexistence of two different hemodynamic patterns may be due to the imbalance resulted from the interaction between alpha-adrenergic responsiveness and beta-adrenergic responsiveness.

Adrenergic alpha-Agonists↗