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Biomedical subjects

C G Strong

Publications and source records attributed to C G Strong.

At least 19 recordsLinked to original sources
PubMed1989

Initial assessment of the patient with hypertension.

The initial assessment of a patient with hypertension can easily be done in a primary-care setting. The goals of the examination are to determine whether the patient is truly hypertensive and, if so, the severity of the hypertension, the degree of target-organ involvement, the presence of curable causes of hypertension, the patient's overall cardiovascular risk profile, and the patient's understanding and willingness to adopt necessary life-style changes and comply with treatment.

Antihypertensive Agents↗
PubMed1988

Parathyroid hormone and calcium. A relationship in hypertension.

Total and ionized calcium, parathyroid hormone, calcitonin, and renin activity were measured in 27 untreated patients with essential hypertension. There was no relationship between any of these parameters and diastolic blood pressure. However, a significant inverse relationship was found between diastolic blood pressure and the ratio of either total or ionized calcium to parathyroid hormone (r = -0.40, P less than 0.05; and r = -0.38, P less than 0.05, respectively). The ratios did not correlate with patient age or plasma renin level. This preliminary finding suggests that the role of plasma calcium in hypertension may need to be analyzed in the context of overall calcium metabolism, as influenced by the parathyroid hormone. The role of an altered relationship between plasma calcium level and parathyroid hormone in the pathophysiology of essential hypertension remains to be studied.

Blood Pressure↗
PubMed1987

Atrial natriuretic peptide in human essential hypertension.

We measured the circulating levels of atrial natriuretic peptide (ANP) in 62 patients with untreated uncomplicated essential hypertension and in 30 normotensive subjects. In the hypertensive patients, mean systolic and diastolic blood pressures were 148 and 101 mm Hg, respectively, and the mean heart rate was 73 beats/min. ANP concentrations were not elevated in the hypertensive group but were actually decreased slightly over those of the control group (27.4 +/- 1.8 pg/ml versus 35.3 +/- 2.4 pg/ml [P less than 0.02]). No relationship was found between ANP levels and diastolic blood pressure, plasma renin activity, urinary sodium excretion, or serum creatinine level. In 8 of the 62 patients with essential hypertension, 6 weeks of treatment with a dihydropyridine calcium channel blocker, nitrendipine, significantly reduced plasma ANP levels from 28.6 +/- 4.3 pg/ml to 18.7 +/- 1.8 pg/ml (P less than 0.05). In 17 additional patients treated with the hypotensive agent ketanserin, ANP levels were not significantly reduced after treatment. Thus, this study demonstrates that circulating plasma ANP levels are not increased but are slightly decreased in patients with uncomplicated essential hypertension in comparison with normotensive subjects. Furthermore, antihypertensive treatment with a calcium channel antagonist reduced plasma levels of ANP.

Adult↗
PubMed1987

Renal parenchymal involvement in essential hypertension.

This article has reviewed the involvement of the kidney as a target organ of essential hypertension. Since Bright first made the association of renal disease and hypertension in 1836, the nature of this relationship has been debated. Although there is evidence implicating abnormalities of renal function in the pathogenesis of essential hypertension, hypertension frequently precedes histologic evidence of alterations in renal structure. Nephrosclerosis, or hardening of the kidney, is the term used to describe the histologic changes occurring in the kidney as the result of hypertension. It can be though of as an acceleration of the normal aging process of the renal vasculature. Glomerular and tubular changes have been traditionally thought to be ischemic in origin. Experimental evidence supports the notion that, as renal function is lost, intraglomerular hypertension develops and may be responsible for additional nephron loss in hypertension. This idea may have therapeutic implications for hypertensive patients with renal insufficiency in that agents that reduce both systemic and intraglomerular pressure may be preferable. Hemodynamically, early hypertension is often characterized by normal peripheral and renal vascular resistance and an increased cardiac output. In established hypertension, cardiac output is usually normal, and peripheral and renal vascular resistances are increased. Renal blood flow is reduced, glomerular filtration rate is maintained, and the filtration fraction rises. In the absence of an accelerated malignant phase, renal failure is uncommon in essential hypertension. Males and blacks are most sensitive to the vascular damage of essential hypertension. Essential hypertension remains an important cause of end-stage renal disease, especially in blacks. Atherosclerotic obstruction of the renal arteries may be a more common cause of renal failure in patients with essential hypertension than has been previously recognized. There are few sensitive markers of early renal involvement in essential hypertension. Several studies of sensitive markers are promising and may detect patients who are prone to renal injury and deserve more aggressive treatment. Malignant hypertension is characterized pathologically by vascular changes of proliferative endarteritis and fibrinoid necrosis. Fortunately, its frequency is decreasing because of early identification and effective treatment of essential hypertension. Effective treatment of severe and malignant hypertension clearly leads to stabilization (and occasionally improvement) of renal function.(ABSTRACT TRUNCATED AT 400 WORDS)

Hemodynamics↗
PubMed1984

Trial of platelet-inhibiting drug in scleroderma. Double-blind study with dipyridamole and aspirin.

In a randomized, double-blind, controlled study, 28 patients with early scleroderma received dipyridamole (225 mg/day) and aspirin (975 mg/day) or placebo for 1-2 years. No significant clinical or objective laboratory improvement was noted in either group. Platelet survival time, plasma renin activity, and coagulation tests were not predictive of disease course. Biomechanical and vascular tests of the hands correlated with clinical extent of skin induration and presence of finger ulcers, respectively.

Aspirin↗
PubMed1978

Renovascular hypertension. Relationship of surgical curability to renin-angiotensin activity.

Fifteen patients whose renovascular hypertension was cured or improved by renal artery reconstructive surgery or nephrectomy (or both) underwent studies of their renin-angiotensin systems preoperatively. These studies included measurements of peripheral venous renin activity in the erect position without diuretic preparation, blood pressure response to blockade of endogenous angiotensin II with a saralasin infusion in the acutely sodium-depleted state, and levels of renal venous renin activity, also after sodium depletion. In 13 of these 15 patients who had benefitted from surgical intervention for relief of renovascular hypertension, at least one index of renin dependency was positive. Two patients had negative results in all of the tests. On the basis of these findings, we concluded that cure or improvement of renovascular hypertension is possible even though these three parameters of renin-angiotensin overactivity are negative.

Angiotensins↗
PubMed1977

Management of the patient with renovascular hypertension.

Renal artery stenosis, either fibromuscular or atheromatous, is probably the most common cause of secondary hypertension in man. Both of these diseases are active, ongoing processes that may be ameliorated but not cured by medical or surgical treatment. The clinical history and examination of the patient with hypertension may help differentiate renovascular hypertension from essential hypertension. The presence of a systolic-diastolic or continuous bruit is often an indicator of severe renal artery stenosis. Systemic hypertension is the physiologic consequence of significant renal artery stenosis. Knowledge of the basic concepts of the renin-angiotensin-aldosterone system, as has evolved from experimental models of renovascular hypertension, forms the basis for understanding the process of evaluation and treatment of such patients. The treatment of choice for the patient with severe hypertension and a functionally significant renovascular lesion is surgical--both in terms of successful treatment of hypertension and improved long-term prognosis. Diligent periodic reevaluation of these patients as well as those with less severe hypertension who are receiving medical treatment enables the physician to select the proper management that offers optimal control of patient blood pressure and avoids target-organ damage to the kidneys, central nervous system, or cardiovascular system.

Humans↗
PubMed1977

The effect of indomethacin blockade of prostaglandin synthesis on blood pressure of normal rabbits and rabbits with renovascular hypertension.

Indomethacin inhibits the synthesis of prostaglandin and the release of renin. These effects were studied in normal rabbits and rabbits with two-kidney Goldblatt hypertension (2KGH) and one-kidney Goldblatt hypertension (1KGH) by giving daily intravenous injections of indomethacin (3mg/kg after two initial doses of 9 mg/kg), and in appropriate control rabbits given diluent phosphate buffer without indomethacin. In normal rabbits, indomethacin significantly decreased immunoreactive plasma prostaglandin E-like substance (IPGE) and plasma renin activity (PRA). Indomethacin did not change plasma creatinine (PCr) or mean blood pressure but it decreased renal blood flow (RBF) and glomerular filtration rate (GFR). In 2KGH rabbits, responses depended on the level of renal function and, to a lesser extent, on the level of PRA. In six of10 2KGH rabbits in which hypertension developed without significant changes in PRA, IPGE, PCr, RBF, and GFR, indomethacin produced changes similar to those seen in normals. In the other four rabbits, development of 2KGH was accompanied by increased PRA, increased IPGE, and decreased RBF and GFR, and indomethacin produced renal failure, oliguria, malignant hypertension, and death within 5 days. In 1KGH rabbits, indomethacin decreased IPGE, PRA, and renal function but increased mean blood pressure. These observations suggest that prostaglandins exert a protective effect on renal function in renovascular hypertension.

Animals↗
PubMed1977

The effect of high sodium intake and angiotensin antagonist in rabbits with severe and moderate hypertension induced by constriction of one renal artery.

The role of renin was assessed in moderate and severe one-clip, two-kidney hypertension in rabbits during normal and high Na intake. Severe hypertension occurred with high levels of plasma renin and creatinine and with extracellular volume depletion. In this group, hypertension was significantly reduced by the 1-hour intravenous infusion of 1,000 ng/kg of an angiotensin II antagonist or by correcting the volume depletion with a high Na intake, which also decreased renin activity and creatinine. The infusion of the antagonist after a high salt diet failed to decrease blood pressure further. Moderate hypertension occurred with plasma levels of renin that were slightly below normal and with no significant abnormalities in extracellular volume depletion or creatinine. In this group, the administration of an angiotensin II antagonist or a high salt diet did not affect any of the three parameters. In normotensive controls, the blood pressure level was not affected by either the angiotensin II antagonist or the high salt diet, despite a reduction in plasma renin activity. Thus, high levels of renin are important in maintaining severe hypertension, and these increased levels probably are accompanied by a concomitant depletion of extracellular volume. Correction of the extracellular volume depletion by a high salt diet is followed by a decrease in renin activity and in blood pressure. In contrast, renin activity does not seem to be important in maintaining moderate hypertension, the pathogenetic mechanism of which remains to be elucidated.

Angiotensin II↗
PubMed1977

Hypertension and the interrelated renal circulatory effects of prostaglandins and the renin-angiotensin system.

Blockade of prostaglandin synthesis with indomethacin (1) did not induce significant changes in blood pressure or in renal circulation in renovascular hypertensive rabbits with normal renal blood flow; (2) induced renal insufficiency and aggravated hypertension in hypertensive rabbits whose renal blood flow was below normal levels; (3) did not alter the reversal of renovascular hypertension produced by the release of the renal arterial constriction; and (4) induced a decrease in plasma renin activity by decreasing renin release. These findings indicate that the vasodilator and natriuretic actions of prostaglandins may play an important role in protecting the kidney against ischemia; the facilitating role of renal prostaglandins on renin release raises the possibility that a primary hypersecretion of renal prostaglandins is responsible for Bartter's syndrome, whereas a primary deficiency may be responsible for "low-renin hypertension."

Angiotensin II↗
PubMed1976

Effects of indomethacin in rabbit renovascular hypertension.

1. Indomethacin inhibits prostaglandin synthesis and interferes with renin release; these effects were studied in rabbit renovascular hypertension. 2. Ten intravenous injections (3 mg day-1 kg-1 after two initial doses of 9 mg/kg) of indomethacin were given daily to ten normal rabbits, ten rabbits with two-kidney Goldblatt hypertension (2KH), tension (1KH). Twelve appropriate control rabbits received diluent phosphate buffer without indomethacin. Plasma renin activity and plasma prostaglandin E2 were measured by radioimmunoassay. 3. In the normal group, indomethacin significantly decreased plasma prostaglandin E2 (1-15 to 0-2 ng/ml, SEM 0-2; P less than 0-01) and plasma renin activity (20 to 3 ng h-1 ml-1, SEM 1, P less than 0-01). Plasma creatinine increased slightly but the mean blood pressure was not significantly changed by indomethacin. 4. Six of ten rabbits with 2KH showed results similar to those in the normal rabbits. In four of ten rabbits in which development of 2KH was accompanied by increments in plasma renin activity (18 to 31-5 ng h-1 ml-1, SEM 3 and 4 respectively; P less than 0-01) and plasma prostaglandin E2 (1-2 to 3-4 ng/ml, SEM 0-2 and 0-4 respectively; P less than 0-05), treatment with indomethacin produced renal failure (plasma creatinine increasing to 7-6 mg/100 ml), oliguria, malignant hypertension (mean blood pressure, 168 mmHg, SEM 7-7) and death within 5 days. 5. In 1KH, indomethacin decreased plasma renin activity and plasma prostaglandin E2, but caused increased mean blood pressure (102 to 121 mmHg, SEM 4 and 6 respectively; P less than 0-01) and decreased renal function (plasma creatinine 0-9 +/- 0-04 to 3-5 +/- 1 mg/100 ml, SEM 0-04 and 1 respectively; P less than 0-01). 6. Aggravation of hypertension was conditioned by pre-existing levels of renal function and, to a lesser extent, by plasma renin activities. 7. These results suggest that prostaglandins exert a protective effect on renal function in renovascular hypertension.

Animals↗
PubMed1976

The effect of indomethacin and other anti-inflammatory drugs on the renin-angiotensin system.

The administration of two different doses of indomethacin, 9 and 18 mg/kg, to two different groups of rabbits was followed 6 h later by a significant decrease in plasma renin activity, and these levels were not increased by hemorrhage. The administration of 2 mg/kg of indomethacin did not alter the basal levels of plasma renin activity, but it was effective in diminishing the peripheral increase of renin produced by hemorrhage. Similar effects were obtained in other groups of rabbits treated with 9 mg/kg of meclofenamate or 18 mg or aspirin. The lowering effect of indomethacin on plasma renin activity is not specifically related to hemorrhage because it also prevented the increase in plasma renin activity elicited by 5 mg/kg of furosemide. Further studies showed that indomethacin did not exert any significant effect in vivo on the plasma level of renin substrate or on the generation of angiotensin from normal plasma by exogenous renin. And indomethacin did not interfere with the binding capacity of anti-angiotensin I for angiotensin I in the radioimmunoassay reaction or with the in vitro formation of angiotensin from hog renin-nephrectomized rabbit plasma reaction. The results thus indicate that the lowering effect of indomethacin on plasma renin activity is due to the interference with renal renin release. That this effect may be related to the blockade of prostaglandin synthesis is suggested by the similar effect exhibited by other blockers of prostaglandin synthesis.

Angiotensin II↗
PubMed1975

Indomethacin enhancement of glycerol-induced acute renal failure in rabbits.

Seventy-three rabbits (2 to 3 kg in weight) were studied during a control period and after receiving 50% glycerol (G) or mercuric chloride (M) with or without indomethacin (I) (controls received the diluent used for I). Plasma creatinine, plasma renin activity, blood pressure, sodium and potassium concentrations, hematocrit value, urinary output, body wt and histologic appearance of the kidney were determined. I enhanced the incidence and severity of the acute renal failure produced by G but failed to aggravate that produced by M. Because the dose of I used in this study blocked the synthesis of renal prostaglandins in the rabbit, we suggest that renal prostaglandins protect against the development of G-induced acute renal failure (a circulatory type of renal failure) in this animal model. Furthermore, the failure of I to aggravate M-induced acute renal failure indicates that it is unlikely that I aggravates G-induced acute renal failure by a direct nephrotoxic effect. No evidence was found for other possible side actions of I being responsible for the observed aggravation.

Acute Kidney Injury↗
PubMed1975

Role of prostaglandins in the reversal of one-kidney hypertension in the rabbit.

Hypertensive rabbits with a clip on the renal artery of their solitary remaining kidney show an abrupt decrease in blood pressure after the arterial constriction is released. Although the mechanism underlying this phenomenon remains controversial, some experimental evidence suggests that it could be humorally mediated. The involvement of prostaglandins was investigated by examining the effect of the release of the arterial constriction on blood pressure, renal blood flow, glomerular filtration rate, and urinary output in five conscious single-kidney hypertensive rabbits in which prostaglandin synthesis was blocked with indomethacin (priming intravenous injection of 9 mg/kg followed by a constant infusion of 1 mg/kg hour-1). The results were compared with those obtained in another group of five single-kidney hypertensive rabbits submitted to the same protocol but not treated with indomethacin. The blockade of prostaglandin synthesis with indomethacin prevented the increments in renal blood flow and glomerular filtration rate seen in the control rabbits after unclipping a significantly retarded the appearance of diuresis and the fall in blood pressure. Despite these observations, the results do not indicate a major participation of prostaglandins in the reversal of single-kidney hypertension, because the decrease in blood pressure 9 hours after the removal of the arterial constriction was similar in both groups.

Aminohippuric Acids↗