Biomedical subjects

N Schork

Publications and source records attributed to N Schork.

23 records · Page 2Linked to original sources

PubMed1988

Effects of ketanserin on blood pressure and platelet aggregation in elderly men with mild hypertension.

Thirteen men, age 60 +/- 2 years (mean +/- SEM) with mild hypertension, 151 +/- 4/95 +/- 3 mm Hg, completed a randomized, double-blind, placebo-controlled crossover trial of ketanserin therapy. In comparison to placebo, ketanserin treatment at 40 mg bid for 6 weeks lowered systolic and diastolic blood pressure, 148 +/- 4/92 +/- 3 vs. 140 +/- 6/86 +/- 3 mm Hg, P = 0.19/0.02. The rate of platelet aggregation in response to ADP and epinephrine was unchanged while the response to serotonin was greatly diminished. Neither the systemic pressor response nor the pupillary mydriatic response to phenylephrine was significantly altered. Plasma norepinephrine concentration declined significantly. Ketanserin reduced blood pressure, particularly the diastolic component, in elderly men with mild hypertension. While antagonism of serotonin's effects on platelet aggregation was evident, blockade of alpha 1-receptor-mediated events was not apparent. The results suggest that during chronic therapy the antihypertensive effects of ketanserin were mediated by serotonergic blockade and a possible lytic effect on sympathetic drive. The dual effects of ketanserin on blood pressure and platelet aggregation may be beneficial in reducing cardiovascular complications in hypertensive patients.

Adult↗

PubMed1988

Sympathetic hyperactivity in early stages of hypertension: the Ann Arbor data set.

Patients with borderline hypertension frequently have a hyperkinetic circulation that is neurogenic and can be normalized with autonomic blockade of the heart. The abnormality is of central nervous system origin and due to increased sympathetic stimulation and decreased vagal inhibition of the heart. A subset of patients characterized by high plasma renin and norepinephrine values clearly has a neurogenic hypertension since their blood pressure becomes normal after cardiac blockade and vascular alpha-adrenergic blockade. Since many patients with borderline hypertension have a high cardiac output, and the majority of patients with more advanced hypertension have increased vascular resistance, two questions arise. Is the "hyperkinetic state" a special condition unrelated to established hypertension or is there, in the course of hypertension, a transition from "high output" to "high resistance" state? The literature strongly suggests that patients with hyperkinetic borderline hypertension later proceed to develop the established high resistance form of hypertension. The most likely mechanism for this transition is a change in cardiac and vascular responsiveness due to prolonged excess sympathetic stimulation combined with structural pressure-induced changes in these organs. This analysis of the events in the course of hypertension is of necessity based on an arbitrary definition of the hyperkinetic state usually set at a cardiac index at least two standard deviations above the normal mean. A bivariate analysis of our data (268 normotensive and 186 patients with borderline hypertension) suggests that there indeed are two different populations in this data set. Based on this commingling analysis, the occurrence of a hyperkinetic state was five-fold as frequent in patients with borderline hypertension than in the normotensive population.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗

PubMed1988

Vascular structure enhances regional resistance responses in mild essential hypertension.

Forearm blood flow (FABF) and forearm vascular resistance (FAVR) responses to sequential regional infusions of norepinephrine (NE) and angiotensin II (Ang II) were examined in 24 hypertensive and 18 matched normotensive subjects. Sensitivity to both vasoconstrictors, defined as the percentage increase in FAVR in response to the lowest dose of each agonist, was similar in the two groups. Also, the FABF response curve to the full range of both agonists did not differ between hypertensives and normotensives by analysis of variance (ANOVA). While the FAVR responses at the lowest doses of both NE and Ang II were similar in hypertensives and normotensives, FAVR responses in hypertensives diverged progressively from the normotensive response pattern, P less than 0.01 according to ANOVA. The hypertensives achieved greater maximum FAVR levels at the highest doses of both agonists, P less than 0.05 according to repeated measures ANOVA. After 10 min of ischaemic exercise, FAVR was higher in hypertensives than in normotensives (2.24 +/- 0.10 versus 1.87 +/- 0.08; P = 0.02, respectively). This value for FAVR was termed the minimum FAVR (mFAVR). The overall response pattern characterized by increased mFAVR, unchanged threshold sensitivity, steeper slope, greater maximum response and similarity of responses to both NE and Ang II is most consistent with a structural augmentation of resistance responses. A model was used in an effort to increase understanding of the vessel morphology. This model suggested that an increased wall/lumen ratio, perhaps without an actual increase in vascular smooth muscle mass, played an important role in the observed FAVR pattern.

Adult↗

PubMed1987

Research utility of noninvasive methods for measurement of cardiac output.

Two noninvasive methods of cardiac index (Q) determination, pulsed Doppler echocardiography (QDop), and CO2 rebreathing (QCO2) were compared to dye dilution in eight normal volunteers. Measurements of Q were made by dye dilution (QDD) and the two noninvasive techniques under the following conditions: supine rest, after inflation of cuffs around the thighs, 35-degree head-up tilt, supine rest repeated, during constant isoproterenol infusion, and after an intravenous bolus of propranolol. When mean Q values of the group for each intervention were compared, close agreement was observed between dye dilution and each noninvasive method (QDOP = 1.08 QDD - 0.07 L/min X m2, r = 0.99, SEE = 0.02; QCO2 = 0.68 QDD + 0.84 L/min X m2, r = 0.97, SEE = 0.02). Fair correlations were achieved when all 48 paired observations were analyzed (QDop = 1.00 QDD + 0.17 L/min X m2, r = 0.89, SEE = 0.17; QCO2 = 0.71 QDD + 0.77 L/min X m2, r = 0.79, SEE = 0.20). However, the Doppler ultrasound technique was significantly more precise in quantitating changes in Q in individual patients. These results demonstrate that estimates of Q can be made with reasonable accuracy by either CO2 rebreathing or Doppler echocardiography. However, the Doppler technique is a much more accurate means of quantitating acute changes in Q.

Adult↗

PubMed1987

Mechanism of increased alpha adrenergic vasoconstriction in human essential hypertension.

Multiple components of vascular alpha adrenergic responsiveness were investigated in twenty-four men with mild hypertension and eighteen age- and weight-matched normotensive controls. Arterial plasma norepinephrine (paNE), an index of sympathetic drive, was increased in hypertensives compared to normotensives (mean +/- SE), 199 +/- 24 vs. 134 +/- 11 pg/ml, P less than 0.02. The effective concentration of intra-arterial (iaNE) increasing forearm vascular resistance (FAVR) 30% (NE-EC30, an index of vascular alpha-receptor sensitivity) was similar in normotensives and hypertensives, 9 +/- 1 vs. 13 +/- 3 ng/100 ml per min, respectively, P greater than 0.3. The phentolamine induced reduction in FAVR, an index of vascular alpha-tone, was greater in hypertensives, -21.3 +/- 1.8 vs. normotensives, -14.9 +/- 1.2 U, P less than 0.02. We interpret these data as evidence for normal vascular alpha-receptor sensitivity to norepinephrine in mild hypertensives. Consequently, the increased sympathetic drive in mild hypertensives explains the elevated vascular alpha-tone. Although vascular alpha-receptor sensitivity to iaNE was normal, the FAVR responses at high doses (reactivity) were greater in hypertensives to regional infusion of both NE and angiotensin II. This "nonspecific" enhancement of vascular reactivity is probably explained by structural vascular changes in hypertensives.

Adult↗