Biomedical subjects

K D Wu

Publications and source records attributed to K D Wu.

At least 55 records · Page 3Linked to original sources

PubMed1993

Atrial natriuretic peptide and blood pressure responses during acute sodium loading in patients with essential hypertension.

Atrial natriuretic peptide (ANP) response during acute saline loading and its relationship to changes in blood pressure (BP) and sodium excretion were studied in 21 patients with essential hypertension (EH) and nine normotensive volunteers. Following 2 liters of isotonic saline infusion at a rate of 500 mL/hour, plasma ANP concentrations in patients with EH increased significantly from 69.9 +/- 6.0 (mean +/- SEM) to 103.6 +/- 17.1 pg/mL (p < 0.05) in the first hour and peaked at the second hour. In normal subjects, the increase in plasma ANP was not significant until the third hour of infusion (64.6 +/- 6.2 to 82.0 +/- 7.5 pg/mL, p < 0.05). Mean BP (MBP) remained stable and the natriuretic responses were similar in the two groups. However, hypertensive patients with a prompt rise in ANP during the initial two hours of infusion (fast responders) maintained a BP balance more efficiently than those with a delayed rise in ANP (slow responders), as the latter displayed a significant increase in MBP two hours after saline loading (126 +/- 5 to 133 +/- 5 mmHg, p < 0.05). Fast responders also had a greater percent of suppression of plasma aldosterone (-49.7 +/- 9.2 vs 15.9 +/- 42.0%, p = 0.05) one hour after saline loading, and a higher increment of natriuresis (263.9 +/- 43.8 vs 97.5 +/- 27.4%, p < 0.025) in the second hour of infusion than slow responders. Our results indicate that during acute saline loading, patients with EH have a faster and greater rise in plasma ANP than normotensives.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Heterogeneous blood pressure response to furosemide and captopril in primary aldosteronism.

The hypertension associated with primary aldosteronism (PA) is often regarded as volume dependent/salt-sensitive. However, not all patients sustain an increase in blood pressure upon sodium loading. In order to examine the sodium sensitivity in PA, 21 patients with aldosteronoma were tested for acute hypotensive response to intravenous furosemide and oral captopril. Ten patients having a decrease in mean blood pressure (MBP) exceeding 5% at the second hour after a 20 mg furosemide injection were defined as diuretic-responders (DR), while the remainder were defined as diuretic-non-responders (DN). The DR group had a higher baseline MBP (135 +/- 6 [mean +/- SE] vs 121 +/- 4 mmHg, p < 0.05) and serum sodium concentration (145.7 +/- 1.4 vs 143.0 +/- 0.7 mmol/L, p < 0.05) than the DN group. The extent of natriuresis induced by furosemide was not different between the two subgroups. Following 100 mg of captopril administered orally, the DR group had a smaller change in MBP (%) than the DN group (3.08 +/- 5.14 vs -7.78 +/- 3.37, p < 0.05). According to the different BP responses to furosemide and captopril, we conclude that PA patients may be further divided into DR and DN. The DR group had a good response to diuretics whereas the DN group responded better to converting enzyme inhibitors. This classification of PA in terms of blood pressure response to furosemide may have therapeutic implications.

Adult↗

PubMed1993

Blood pressure response to angiotensin converting enzyme inhibitor in essential hypertension: its relation to the renin status and natriuresis during acute sodium loading.

We examined the antihypertensive response to enalapril and its relation to the changes of the renin-angiotensin-aldosterone axis (RAA) in essential hypertensive patients. The responders, whose blood pressure reduced after enalapril administration, had significant elevation of plasma renin activity after enalapril (7.5 +/- 4.0 to 31.9 +/- 10 ng/mL/h, p < 0.05). There was no significant change in the plasma renin activity of the nonresponders (3.0 +/- 1.0 to 5.6 +/- 1.9 ng/mL/h). Natriuretic response to acute salt loading was compared between the two subgroups. The natriuresis on acute salt loading of nonresponders was better than that of the responders (82.9 +/- 13.2 vs 44.5 +/- 5.7 mmol/4h, p < 0.05). These results imply that the RAA and extracellular fluid volume both contribute in different ways to the maintenance of high blood pressure in different subgroups of essential hypertension.

Adult↗

PubMed1993

Renin suppressibility and blood pressure response during acute sodium loading in patients with essential hypertension.

Sequential changes in renin-aldosterone secretions and blood pressure (BP) response during acute sodium (Na) loading were studied in 50 patients with essential hypertension (EH) and nine normotensive volunteers. Following an infusion of 2 L of isotonic saline at a rate of 500 mL/h, plasma renin activity (PRA) and the plasma aldosterone concentration (PAC) were similarly suppressed, while sodium excretion appreciably increased in hypertensive as well as normotensive subjects. When patients were divided into two subgroups according to the extent of renin suppression, 26 were classified as adequate responders with the proportion of decrement of PRA at the end of the infusion exceeding 50% of the baseline values, while 24 were inadequate responders with a decrement of less than 50%. The extent of renin suppression was consistently greater in adequate responders than in inadequate responders throughout the course of infusion. Adequate responders also had a higher pre-saline PRA and attained a smaller post-saline natriuretic response than inadequate responders. Although the mean BP in both subgroups remained stable at all periods, inadequate responders had a minor but significantly higher percent of increment of MBP at the end of the infusion than adequate responders (3.6 +/- 2.0 vs -1.7 +/- 1.4%, p < 0.05). These results suggest that renin suppressibility during acute Na loading may be either linked with maintenance of BP homeostasis or may merely reflect the sodium-volume status of essential hypertension, with patients with greater suppression of renin being more Na-volume resistant than those with less inhibition.

Adult↗

PubMed1992

[Blood pressure and metabolic response to converting enzyme inhibitor in hypertensive patients: comparison between delapril and captopril].

The antihypertensive and metabolic responses to delapril and captopril in hypertensive patients were studied. Forty-six hypertensive patients entered the study and were divided into two groups. The delapril group included 21 essential hypertensive and five renoparenchymal hypertensive patients; while the captopril group included 11 essential hypertensive and nine renoparenchymal hypertensive patients. The patients in the delapril group took delapril 7.5 mg twice a day for 2 weeks. If the antihypertensive effect was inadequate, the dose was increased to 15mg twice a day, and then to 30mg twice a day. The period of delapril treatment was 12 weeks. The patients in the captopril group took captopril 25 mg twice a day or three times a day for 12 weeks. After delapril treatment, there were significant decreases in the systolic (from 163 +/- 17 to 141 +/- 15 mmHg) and diastolic blood pressure (from 105 +/- 13 to 91 +/- 10 mmHg). There were also significant decreases in the systolic (from 161 +/- 18 to 141 +/- 24 mmHg) and diastolic blood pressure (from 100 +/- 10 to 90 +/- 12 mmHg) after captopril treatment (p < 0.001). The pulse rates in both groups showed no significant changes after treatment. The laboratory data in both groups showed few changes after treatment. Plasma renin activity increased after delapril treatment. A cough was the side effect most commonly seen. We conclude that hypertensive patients have the same blood pressure and metabolic responses to delapril as captopril.

Adult↗

PubMed1991

Plasma active renin, inactive renin and kallikrein in patients with disseminated intravascular coagulation.

To investigate the role plasma kallikrein plays in the in vivo activation of inactive renin, we measured plasma active renin, inactive renin, kallikrein and prekallikrein levels in 10 patients with disseminated intravascular coagulation (DIC), with 16 normal persons as controls. The plasma active renin concentration was expressed by the angiotensin I generation rate after the addition of sheep renin substrate. Plasma inactive renin was activated by trypsin. The plasma total kallikrein level was measured by an assay of kallikrein activity on synthetic substrate S-2302 after the addition of a prekallikrein activator. Plasma kallikrein was assayed by its activity on S-2302 without addition of the activator. The prekallikrein level was obtained by subtracting the kallikrein activity from the total kallikrein activity. A significant decrease in the plasma prekallikrein concentration was observed in DIC patients, as compared to that of controls (p less than 0.01). There was no significant difference in plasma levels of kallikrein, inactive renin, and the proportion of active renin between DIC patients and normal controls, but the active renin level was higher in DIC patients. There was no significant correlation between the level of plasma kallikrein and the proportion of active renin in either normal controls or DIC patients. These results are compatible with, but do not prove, the theory that plasma kallikrein plays a role in the in vivo activation of inactive renin.

Adolescent↗

PubMed1991

A plasma factor participates in the cryoactivation of plasma inactive renin.

Plasma inactive renin (IR) can be cold activated (-4 degrees C). This process is called cryoactivation. The mechanism of cryoactivation is not yet elucidated. To investigate the mechanism of cryoactivation, we initially determine the isoelectric point (pI) of plasma active renin (AR) and IR by means of isoelectric focusing. The electrofocusing was performed in a LKB 8100-1 column containing a sucrose gradient and pH 3.5-10 ampholine under 4 degrees C. We found that the pI of AR was 5.0 and 3.9 whereas the pI of IR was 5.6. By using pH 4-6 ampholine, we separated IR from AR and added all fractions containing only IR to each of the electrofocusing column eluates (pH 4-6 ampholine). We found there was no increase in renin activity. If each fraction of electrofocusing eluate (after pH 4-6 ampholine) was cryoactivated, without adding the IR containing fractions, a small increase in angiotensin I (AI) generation was seen in the fractions of pH 4.9-5.1. However, when eluates from the electrofocusing column using pH 3.5-10 ampholine were added to fractions containing only inactive renin, and cryoactivation was subsequently performed, a peak increase in AI generation was found in the fractions corresponding to pH 4.9-5.1. Therefore, cryoactivation may expose certain enzyme(s) which have the pI of 4.9-5.1 and can activate inactive renin. We further found that these fractions could split the synthetic substrate S-2302. Such an activity may be produced by plasmin or related enzymes.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin I↗

PubMed1991

Exaggerated natriuresis in primary aldosteronism.

Acute response in blood pressure (BP) and natriuresis to saline infusion was evaluated in 16 patients with primary aldosteronism caused by aldosteronoma (PA) and 12 patients with salt-sensitive essential hypertension (SSEH). Salt-sensitivity was defined by a decrease in mean BP exceeding 5% at the second hour after a 20 mg furosemide injection. Plasma renin activity (PRA), plasma aldosterone concentration (PAC) and urine electrolytes in response to saline infusion were determined. During a 2-liter isotonic saline infusion, a similar degree of natriuresis and change in BP were observed in PA and SSEH patients. A significantly inverse correlation between the increase in mean BP and the degree of natriuresis at the end of the infusion was found in patients with SSEH (r = -0.80, p less than 0.01). No correlation was observed between these parameters in patients with PA (r = 0.28, p greater than 0.05). These results suggest that hypernatriuresis in SSEH may play a protective mechanism against abrupt increases in BP and volume during acute saline loading. This protective mechanism was not evident in patients with PA.

Adrenal Cortex Neoplasms↗

PubMed1990

Exaggerated natriuresis in salt-sensitive essential hypertension.

Acute responses of blood pressure and natriuresis to intravenous injection of furosemide and saline infusion were evaluated in 38 patients with essential hypertension. Twelve patients whose mean arterial blood pressure decreased by more than 5% at two hours after intravenous administration of 20 mg furosemide were classified as salt-sensitive (SS); the remainders as salt-resistant (SR). The extent of natriuresis induced by furosemide was not different between the two subgroups. During 2-liter isotonic saline infusion the SS subjects excreted more sodium than the SR subjects did (108.7 +/- 11.9 vs 55.9 +/- 6.6 mmole, p less than 0.001). There was a significant correlation (r = 0.57, p less than 0.001) between the hypotensive effect of furosemide and the 4-hour sodium excretion during saline infusion. A reverse correlation between the sodium excretion during saline infusion and the increase in mean blood pressure at the end of infusion was shown in the SS subgroup (r = -0.72, p less than 0.01), but not in the SR subgroup (r = 0.045). The results suggest that prompt natriuresis on saline infusion in the SS hypertensives may function as a protective mechanism to prevent abrupt increase in blood volume and blood pressure during acute sodium loading.

Adult↗

PubMed1990

A simulation study on renin and aldosterone secretions in primary aldosteronism.

A system dynamics modeling method was developed to predict changes in plasma renin activity (PRA), plasma aldosterone (PA) and electrolyte concentrations in response to diuretic stimulation in patients with primary aldosteronism. Its clinical validity was evaluated by comparing experimental and simulation results. In a clinical experiment, furosemide 20 mg was given by intravenous injection to 20 patients with primary aldosteronism. PRA, PA and electrolyte concentrations were measured hourly for 3 hours after administration of the drug. The computer simulation outputs were consistent with the experimentally measured values at each corresponding point of time. An analysis of model predictions indicates that the method may predict the changes in PRA, PA and electrolyte concentrations after diuretic administration in accordance with a time interval.

Aldosterone↗

PubMed1988