Haemodynamic and Endocrine Responses of the Kidney to Frusemide in Mild Essential Hypertension

Mackay, I. G.; Nath, Karl A.; Cumming, Allan D.; Muir, Alexander; Watson, M.

doi:10.1042/cs0680159

Cited by 11 publications

(4 citation statements)

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“…These stimuli induce secondary aldosteronism, which probably alters renal synthesis and release of kallikrein in the long term [2 1,251. Urinary kallikrein excretion is reduced in patients with primary hypertension [26]. However, this may be secondary to renal damage induced by the hypertensive state, since normal kallikrein excretion has also been reported in patients with mild hypertension [27]. The only sign of renal damage in the hypertensive patients in our study was a lower fasting morning urine osmolarity.…”

Section: Discussionsupporting

confidence: 45%

“…Several studies on the effects of frusemide on urinary kallikrein and prostaglandins have also been performed in humans [24,27,301. Stimulation of prostaglandins by frusemide appears to mediate increased renal blood flow [31], but it has been difficult to link specific renal excretory effects of frusemide to either kallikrein or prostaglandins.…”

Section: Discussionmentioning

confidence: 99%

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Plasma and tissue kallikrein–kinin systems during acute administration of frusemide in normotensive and hypertensive humans

Öhman¹,

Karlberg²

1991

Clinical Science

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1. This study aims to further elucidate the role of the tissue and plasma kallikrein-kinin systems in blood pressure, electrolyte and volume homoeostasis. Components thereof and of the renin-angiotensin-aldosterone system were measured in conjunction with frusemide administration, in normotensive subjects and in patients with primary hypertension. 2. Frusemide increased plasma pre-kallikrein, angiotensin II and aldosterone concentrations and plasma renin activity, whereas the plasma level of tissue kallikrein remained unchanged. Basal values and the induced changes were similar in both groups. 3. Frusemide increased the urine volume and the excretion of Na+, K+, Mg2+, Cl-, aldosterone, prostaglandin E2 and tissue kallikrein. These changes were similar in both groups, but the total tissue kallikrein excretion was significantly lower in the hypertensive patients. Excretion of electrolytes and hormones was also measured during three 24 h urine collection periods and did not differ between the two groups. 4. Thus, acute administration of frusemide to hypertensive patients and normal subjects increased the plasma level of pre-kallikrein, possibly indicating less activation to kallikrein and subsequently less kinin generation in the blood stream. This also suggests a role for the plasma kallikrein-kinin system in the regulation of vascular tone and blood volume. Circulating tissue kallikrein does not seem to be acutely involved. 5. Urinary excretion of kallikrein is reduced in patients with primary hypertension after the administration of frusemide, apparently without affecting the renal excretory response.

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Section: Discussionsupporting

confidence: 45%

Section: Discussionmentioning

confidence: 99%

Plasma and tissue kallikrein–kinin systems during acute administration of frusemide in normotensive and hypertensive humans

Öhman¹,

Karlberg²

1991

Clinical Science

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“…In this regard it is interesting to note that the natriuretic response to furosemide (with which atrial peptides have been compared) is by contrast the same or less in hypertensive patients compared with that in normotensive subjects. 13 " 15 Second, the hypertensive subjects had little or no fall in arterial pressure apart from the brief hypotensive response immediately after a-hANP injection. This response contrasts with the small but sustained decline in pressure in the normotensive volunteers previously studied using the same measurement technique.…”

Section: Fioure 6 Relation Between the Mean Intra-arterial Pressure mentioning

confidence: 99%

Effects of alpha-human atrial natriuretic peptide in essential hypertension.

Richards¹,

Nicholls²,

Espiner³

et al. 1985

Hypertension

131

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Because there is little published information on the effects of atrial peptides in hypertensive humans, 100 micrograms of alpha-human atrial natriuretic peptide was injected intravenously into six patients with essential hypertension in a double-blind, placebo-controlled study under standardized conditions of body posture and dietary sodium and potassium intake. The peptide increased urine sodium excretion sixfold in the first 30 minutes. Smaller increments occurred in urine volume and in calcium, magnesium, and phosphorus excretion; the rise in urine potassium concentration was not statistically significant. Most of these indices returned to time-matched placebo values within 1 hour, but urine sodium excretion remained high for 2 1/2 hours. Arterial pressure fell within 2 minutes of alpha-human atrial natriuretic peptide injection, then returned to matching placebo levels by 10 minutes. Conversely, heart rate increased rapidly and remained elevated for 3 hours. The peptide induced a prompt, brief rise in plasma norepinephrine concentration and a more sustained fall in epinephrine and aldosterone levels, but it did not affect plasma renin activity or cortisol concentration. Compared with normotensive volunteers studied previously under the same conditions, the hypertensive subjects had a greater response in urine volume and sodium, calcium, and magnesium excretion but a less sustained fall in arterial pressure.

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“…We have observed pa tients in whom UKa has fallen to normal following effec tive diuretic therapy, but this has not been uniformly seen [Cumming, unpubl. observations], and the known stimu lating effect of most diuretics on the renal kallikreinkinin system makes interpretation of these findings diffi cult [20], Studies of kallikrein excretion in other oedematous states would be of interest in this regard; patients with alcoholic cirrhosis of the liver excrete less urinary kallikrein than normal, despite dietary sodium restriction and severe oedema and ascites [21]. The possibility exists that hypoproteinaemia per se could influence kallikrein excretion, perhaps by an effect on delivery of sodium to the distal nephron [22,23].…”

Section: Discussionmentioning

confidence: 99%

The Kallikrein-Kinin and Renin-Angiotensin Systems in Nephrotic Syndrome

Cumming¹,

Jeffrey²,

Lambie³

et al. 1989

Nephron

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We previously found that virtually all patients with nephrotic syndrome (NS) excrete supranormal amounts of urinary kallikrein; it is known that activity of the renin-angiotensin system (RAS) is increased in some such patients. We therefore studied the relationship between urinary kallikrein excretion (U_Ka) and plasma renin activity (PRA) in 16 patients with NS. Compared with healthy controls, PRA was normal in 8 subjects and elevated in 8; U_Kawas elevated in the high-renin group (40.4 ± 5.2 nkat/24 h, normals 12.0 ± 1.1). U_Ka was also elevated in the normal renin group (25.7 ± 2.4 nkat/24 h) but to a significantly lesser degree. Significant activity in plasma against a specific substrate of glandular and renal kallikreins was observed in 8 of 10 patients with NS. Such activity was not found in plasma of 17 patients with glomerulonephritis without NS, or in 10 healthy controls. The results are in keeping with previous suggestions of a functional link between the renal kallikrein-kinin system (KKS) and the RAS, but indicate that the renal KKS is activated in NS, in some cases independently of the RAS. It is possible that renal kallikrein reaches the systemic circulation in some patients with NS.

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Haemodynamic and Endocrine Responses of the Kidney to Frusemide in Mild Essential Hypertension

Cited by 11 publications

References 0 publications

Plasma and tissue kallikrein–kinin systems during acute administration of frusemide in normotensive and hypertensive humans

Plasma and tissue kallikrein–kinin systems during acute administration of frusemide in normotensive and hypertensive humans

Effects of alpha-human atrial natriuretic peptide in essential hypertension.

The Kallikrein-Kinin and Renin-Angiotensin Systems in Nephrotic Syndrome

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