Prostaglandin System Research Articles

Long-Lasting Depression of Rabbit Aortic Prostacyclin Formation by Single-Dose Irradiation

Male rabbits were exposed to a single irradiation dose of 1000-5000 rad when 12, 15, 16, and 17 months old and were killed when 18 months old (i.e., 1, 2, 3, and 6 months after irradiation). Even after this long interval after irradiation, abdominal aortic prostacyclin formation was significantly depressed, whereas the nonirradiated thoracic aortic segment exhibited no significant alteration in vascular PGI2 generation. The data show that the severe decrease in PGI2 synthesis was not caused by deendothelialization induced by irradiation alone. The data support the view that a deterioration in the prostaglandin system regulating hemostatic balance is an important determinant in the development of radiation-induced vasculopathy.

Renin release induced by a nonvasoconstrictor dose of phenylephrine is independent of the renal prostaglandin system in anesthetized dogs.

We examined the relationship between prostaglandin (PG) production and renin release induced by a nonvasoconstrictor dose of an alpha-agonist, phenylephrine, in anesthetized dogs. Intrarenal infusion of phenylephrine (1 microgram/min) did not affect systemic blood pressure or renal blood flow, but increased the renin secretion rate about twofold. The effect of phenylephrine on renin release was abolished by the intrarenal infusion of the alpha-antagonist phentolamine (50 micrograms/min), but was not affected by the intravenous administration of the PG synthetase inhibitor indomethacin (5 mg/kg). Urine flow and urinary sodium excretion rate were not altered by phenylephrine. These results suggest that a nonvascular and nontubular alpha-adrenoceptor mechanism, which is independent of the renal PG system, may be involved in renin release.

Is the cardiovascular effect of nitroglycerin related to the prostaglandin system in the dog?

Is the cardiovascular effect of nitroglycerin related to the prostaglandin system in the dog?

Plaque-forming cells in man. IV. Influence of acetylsalicylic acid in vivo and dexamethasone in vitro.

The influence of acetylsalicylic acid (ASA) and steroid (ST) on the number of plaque-forming cells (PFC) developed in pokeweed mitogen-activated cultures of peripheral blood lymphocytes (PBL) was investigated. Cultures of 10(6) PBL were established from blood samples of 16 healthy volunteers before and after intake of 2 g of ASA, and parallel cultures were supplemented with ST in vitro. The immunoglobulin secretion was monitored with a protein A assay. Our results show that pharmacological doses of ASA in vivo decrease the number of PFC by 41%, whereas the distribution of the subpopulations was unaltered. In cultures of PBL obtained before the intake of ASA and supplemented with 10, 50 or 100 micrograms/ml of dexamethasone the number of PFC was decreased by 50%, 41% and 44%, respectively. In cultures of PBL obtained after the intake of ASA and supplemented with 10, 50 or 100 micrograms of ST, the number of PFC was further decreased by 22%, 32% and 38%. The effects of ASA in vivo and ST in vitro were additive. The ratio of IgM, IgG and IgA PFC was unaffected by ASA and ST. It is suggested that the modulation of the PFC response induced by ASA and ST is mediated by the prostaglandin system.

Interrelationships between the renal kallikrein-kinin and prostaglandin systems in furosemide-induced diuresis.

The relationships between the renal kallikrein-kinin (K-K) and prostaglandin (PG) systems under conditions of furosemide-induced diuresis were studied in normal rats. Urinary PGE and PGF2 alpha were measured by radioimmunoassay, and urinary kallikrein by enzymatic activity. The diuretic and natriuretic effects of furosemide were accompanied by a concomitant increase in the urinary excretion of kallikrein and PGE. The urinary excretion of kallikrein and PGE was closely related to the urinary excretion of sodium, potassium and chloride. The urinary excretion of kallikrein also showed a highly significant correlation with the urinary excretion of PGE. Pretreatment of the animal with indomethacin or aprotinin inhibited furosemide-induced diuresis and natriuresis. Aprotinin inhibited the urinary excretion of PGE, while indomethacin did not exert any inhibitory action on the urinary excretion of kallikrein. Although the urinary excretion of kallikrein was closely related to the urinary excretion of potassium, both indomethacin and aprotinin had no effect on the urinary excretion of potassium. The results indicate that the potassium-sodium exchange caused by furosemide in the distal nephron might stimulate the renal K-K system to result in increasing synthesis of PGE, which would, at least in part, participate in the diuretic and natriuretic effects of furosemide.

Prevention of interstitial pressure change at unilateral nephrectomy by prostaglandin synthesis inhibition

AbstractPrevention of interstitial pressure change at unilateral nephrectomy by prostaglandin synthesis inhibition. The mechanisms underlying the adaptive process in the remaining kidney after unilateral nephrectomy are not well known. In the present study adaptive changes in interstitial pressure conditions following uninephrectomy were investigated in male Sprague-Dawley rats. Direct subcapsular hydrostatic pressure recordings were made via microcatheters, renal lymph was collected for lymph flow rate estimations and determinations of lymph protein content and the urine flow rate and urinary excretion of sodium and potassium were measured, before and after contralateral nephrectomy. There was a significant rise in subcapsular hydrostatic pressure by about 50%, and in the lymph flow rate, by more than 100%, within 1 hr after nephrectomy. The protein concentration in collected renal lymph was significantly decreased (from 2.30 ± 0.25 to 1.45 ± 0.26 g/dl), compared with control collections in sham-operated animals (from 2.22 ± 0.23 to 1.78 ± 0.19 g/dl). These findings indicate an increased hydrostatic and decreased interstitial pressure in response to contralateral nephrectomy. Urine flow rate and electrolyte excretion were significantly elevated (urine flow rate by 92%, sodium excretion from 0.210 ± 0.035 to 0.352 ± 0.067 µmoles/min and potassium excretion from 0.306 ± 0.074 to 1.617 ± 0.228 µmoles/min). Inhibition of prostaglandin synthesis prior to nephrectomy abolished the lymph flow increase and oncotic pressure decrease and also the diuretic and natriuretic responses. The adaptively increased potassium excretion was, however, only blocked by diclofenac sodium and not by indomethacin. These results demonstrate the important role of the renal interstitium and the prostaglandin system in the renal adaptation to nephron loss.Prévention des modifications de pression interstitielle lors d'une néphrectomie unilatérale par inhibition de la synthèse des prostaglandines. Les mécanismes responsables des phénomènes d'adaptation dans le rein restant après néphrectomie unilatérale ne sont pas bien connus. Dans cette étude, les modifications adaptatives des conditions de pression interstitielle après uninéphrectomie ont été étudiées chez des rats mâles Sprague-Dawley. Des enregistrements directs de la pression hydrostatique sous-capsulaire ont été effectués par des micro-cathéters, de la lymphe rénale été collectée pour des estimations du débit lymphatique et des déterminations des protéines lymphatiques, et le débit urinaire et l'excrétion de sodium et de potassium ont été mesurés, avant et après néphrectomie controlatérale. Il y avait une élévation significative de la pression hydrostatique sous capsulaire d'environ 50%, et du débit lymphatique de plus de 100%, dans 1 heure suivant la néphrectomie. La concentration protéique dans la lymphe rénale collectée était significativement diminuée (de 2,30 ± 0,25 à 1,45 ± 0,26 g/dl), par rapport aux collections contrôles chez les animaux ayant subi un simulacre d'opération (de 2,22 ± 0,23 à 1,78 ± 0,19 g/dl). Ces résultats indiquent une augmentation de la pression hydrostatique et une diminution de la pression interstitielle en réponse à une néphrectomie controlatérale. Le débit urinaire et l'excrétion d'électrolytes étaient significativement élevés (le débit urinaire de 92%, l'excrétion sodée de 0,210 ± 0,035 à 0,352 ± 0,067 µmoles/min et potassique de 0,306 ± 0,074 à 1,617 ± 0,228 µmoles/min). L'inhibition de la synthèse de prostaglandines avant le néphrectomie a aboli l'élévation du débit lymphatique et la baisse de la pression oncotique ainsi que les réponses diurétique et natriurétique. L'augmentation adaptative de l'excrétion potassique était toutefois seulement bloquée par le diclofénac sodique et non par l'indométhacine. Ces résultats démontrent le rôle important de l'interstitium rénal et du système des prostaglandines dans l'adaptation rénale à la perte néphronique.

Facilitating interaction between rauwolscine and angiotensin in the mesenteric artery of the rabbit.

The interaction between rauwolscine and angiotensin II was investigated in the isolated mesenteric artery of the rabbit. Rauwolscine, known as an antagonist at alpha 2-adrenoceptors, did not induce contraction itself but interacted with angiotensin to produce a facilitated response of the vascular tissue. In the presence of rauwolscine, the contractile response of the tissue to angiotensin was markedly enhanced. The degree of facilitation appeared to be dependent on the rauwolscine concentration used rather than that of angiotensin. Moreover, rauwolscine induced a concentration-dependent increase in tension (pD2 = 6.8) in the presence of even subcontractile concentrations of angiotensin (10(-10) mol/l). This effect was not attributable to an indirect action involving presynaptic catecholamines, as revealed by the use of tissue strips from animals pretreated with reserpine or after chemical sympathectomy. Furthermore, an interaction via the prostaglandin system was excluded by negative results obtained with indomethacin. The 'agonistic effect' of rauwolscine was significantly attenuated by phentolamine (alpha 1/alpha 2) but not by prazosin (alpha 1) or phenoxybenzamine when applied for only a short time. The alpha 2-antagonist BDF 6143 behaved like rauwolscine whereas the alpha 1-antagonist corynanthine, a stereoisomer of rauwolscine, did not. The results indicate that the 'rauwolscine effect' is mediated by a receptor with alpha 2-characteristics. In general, angiotensin appears to interfere with some process which determines the expression of a drug's intrinsic effect.

Role of the renal prostaglandins in furosemide-induced diuresis.

The role of the renal prostaglandin (PG) system in the renal effects of furosemide was assessed by using indomethacin, an inhibitor of PG synthetase, in conscious rats under conditions of vasopressin infusion (or dehydration). Urinary PGE and PGF2 alpha were measured by radioimmunoassay under conditions of furosemide-induced diuresis. The diuretic and natriuretic effects of furosemide were accompanied by a concomitant increase in the urinary excretion of PGE. In normal rats the pretreatment of indomethacin at 10 mg/kg failed to alter the diuretic effect of furosemide (5 mg/kg). In contrast, the diuretic effect of furosemide in vasopressin (2 U/kg)-infused (or dehydrated) rats was greatly inhibited by indomethacin. In regard to the natriuretic effect of furosemide, indomethacin did impair this response to furosemide both in normal and vasopressin-infused (or dehydrated) rats, but inhibited more strongly in the latter than in the former. These results suggest that the renal PGE is necessary for furosemide to produce optimal diuretic and natriuretic effects under conditions of vasopressin infusion (or dehydration).

Prostaglandins and hypertension.

The level of arterial blood pressure is set by a complex interrelationship of several mechanisms which influence both blood flow in and resistance of the vascular system. An imbalance which favours those mechanisms that elevate vascular resistance or extracellular volume will result in hypertension. Such alterations may include increased activity of the adrenergic nervous system, of the renin angiotensin system, or excessive secretion of mineralocorticoids. Of equal importance may be an underactivity of blood pressure lowering factors, such as prostaglandins and the kallikrenin-kinin-system. A deficiency of the vasodepressor systems may lead to hypertension even without an increase in the activity of the blood pressure elevating systems. Beside a genetic predisposition, exogenous risk factors are assumed to play a major role in the natural history of essential hypertension and arterial vascular disease. The contribution of prostaglandins to the etiology of these cardiovascular disorders may be based on an inherent abnormality of the prostaglandin system as well as on the effects of major risk factors such as dietary intake of sodium and fat on prostaglandin formation.

Effects of a selective thromboxane A2 synthetase inhibitor on immune complex glomerulonephritis.

It has been reported that agents which block the prostaglandin system inhibit the development of glomerulonephritis. However, the mechanisms of these effects are not clear. We studied the effect of a selective thromboxane A2 (TxA2) synthetase inhibitor, 1-benzylimidazole (BIm), on the immune complex glomerulonephritis produced by bovine serum albumin (BSA) in New Zealand white rabbits. As the BSA nephritis developed, there was no change of creatinine (Cr), serum urea nitrogen (SUN), or creatinine clearance (Ccr), but urinary protein excretion increased almost 3-fold. Coagulation and fibrinolytic studies suggested a hypercoagulable state and increased fibrinolytic activity. Platelet aggregation showed the reduction of maximum aggregation induced by ADP and collagen. Histological examination by light microscopy, immunofluorescence, and electron microscopy revealed glomerular polymorphonuclear leukocyte (PMN) infiltration, mononuclear cell (MON) proliferation, and fibrin deposition. In 70% of the rabbits, IgG and C3 deposits were seen by immunofluorescence mainly in mesangial areas. The administration of BIm to BSA nephritis had no effects on Cr, SUN or Ccr, but it significantly lessened the proteinuria. The study of coagulation and fibrinolytic activity suggested a less hypercoagulable state, and more efficient fibrinolysis occurred than in the group without BIm. BIm tended to normalize platelet aggregation. It also lessened the histological PMN infiltration (p less than 0.05), MON proliferation (p less than 0.01), and fibrin deposition (p less than 0.05). These data suggest that TxA2 may play an important pathogenetic role in the development and progression of glomerulonephritis.

Influence of adrenergic nervous and prostaglandin systems on hydralazine-induced renin release

The role of the β-adrenergic nervous and prostaglandin systems in vasodilator-induced activation of the renin-angiotensin system was studied in conscious rats. The plasma renin activity (PRA) response to intravenous hydralazine (0.25, 0.5 and 1 mg/kg body wt.) was compared to the PRA response following administration of similar doses of hydralazine to rats pretreated with either indomethacin (3 mg/kg body wt. i.v.) or indomethacin and propranolol (1 mg/kg body wt. i.v.). PRA increased significantly above control levels after each of the hydralazine doses. In rats pretreated with indomethacin, PRA did not increase with the 0.25 mg/kg dose of hydralazine; increased significantly with the 0.5 mg/kg dose but remained significantly lower than the PRA response in the absence of indomethacin; and increased with the 1 mg/kg dose to a level not significantly different from PRA in rats receiving only hydralazine. When rats were pretreated with indomethacin and propranolol, PRA did not increase significantly in response to either the 0.25 or 0.5 mg/kg doses of hydralazine. Although a statistically significant increase in PRA was noted with the 1 mg/kg dose of hydralazine, the level of PRA achieved was very low and only 15% of that observed with the other two treatment regimens (i.e., hydralazine alone or indomethacin and hydralazine). These results demonstrate that vasodilator-induced renin release is only partially mediated via the prostaglandin system, that the degree of this control is related to the intensity of vasodilator stimulus and that renin release following administration of hydralazine can be attributed almost entirely to activation of the β-adrenergic nervous and prostaglandin systems.

The systemic beta-adrenergic pathway to renin secretion: relationships with the renal prostaglandin system.

The relationship between renin release evoked by circulating beta-agonists and the renal prostaglandin (PG) system is incompletely defined. Thus, we evaluated systemic and renal hemodynamic responses to iv (0.5 micrograms/kg X min) and intrarenal arterial (0.6 micrograms/kg X min) infusions of the beta1-agonist prenalterol (PNL) in four separate groups of anesthetized dogs. Consecutive iv PNL infusions (n = 6) resulted in a reversible decrease in mean arterial pressure (130 to 117 mm Hg; P less than 0.05) and increases in cardiac output (3.93 to 4.90 liters/min; P less than 0.001), PRA (1.96 to 5.12 ng/ml X h; P less than 0.01), and 6-keto-PGF 1 alpha levels (190 to 482 pg/ml; P less than 0.01). The glomerular filtration rate and renal blood flow were modestly, but not significantly, decreased by the PNL infusions. In a second group of dogs, the infusion of the PG synthesis inhibitor indomethacin (IN; 10 mg/kg, iv; n = 7) before the second PNL infusion blunted PG increases but did not significantly modify the systemic or renal hemodynamic responses to PNL. The magnitude of the PRA and renin secretory rate (RSR) increases post-IN administration was similar to control values, but the absolute levels achieved were not as great as before IN infusion. To assess the role of the renal baroreceptor pathway to renin release after PNL, a suprarenal clamp was used to maintain a constant renal perfusion pressure during PNL infusion in a third group of dogs. In this group (n = 5), both PRA and RSR (from innervated and denervated kidneys) increased after PNL infusion, although IN again diminished the maximum PRA and RSR responses observed. Finally, the unilateral intrarenal arterial infusion of PNL in the last group of dogs did not alter PRA, RSR, or renal hemodynamics. These results demonstrate that renin release elicited by a circulating beta-agonist functions independently of PG synthesis, and that the pathway operates via an extrarenal mechanism.

Is the cardiovascular effect of nitroglycerin related to the prostaglandin system in the dog?

Open-chest dogs were used for studies of the effects of intra-coronary (0.3–10 μg) or i.v. nitroglycerin (0.3–100 μg/kg) on systemic blood pressure (SBP), heart rate, left ventricular (LV) pressure, coronary blood flow and vascular resistance in the absence of presence of indomethacin (3 mg/kg i.v.). The nitroglycerin-induced changes in the cardiovascular parameters were not sifnificantly modified by indomethacin (3 mg/kg i.v.). The dose of indomethacin used was large enough to inhibit significantly, for more than 2 h, the coronary vasodilation induced by arachidonic acid (100 μg) administered intra-arterially. The present study suggests that the cardiovascular action of nitroglycerin may not be mediated through the prostaglandin system.

Effects of indomethacin and ibuprofen on cerebral metabolism and blood flow in traumatized brain.

Local cerebral glucose utilization (LCGU) and local cerebral blood flow (LCBF) were studied by autoradiographic techniques in indomethacin- and ibuprofen-treated rats with focal cortical freezing lesions. Widespread depression of LCGU, which developed with time after the lesion in untreated animals was significantly diminished by the prostaglandin synthetase inhibitors indomethacin (single injection 7.5 mg/kg) and ibuprofen (36 mg/kg/day). Both drugs were effective when given 6 h before or up to 24 h after the lesion was made. The effect of the drugs was most striking in cortical areas of the traumatized hemisphere, where the depression was most profound in untreated animals. Thus, 3 days after the lesion, average LCGU in these regions was 46%, 86%, and 98% of normal in untreated, indomethacin-pretreated, and ibuprofen-pretreated rats, respectively. Prostaglandin formation was completely inhibited in the lesion area in the indomethacin-treated rats (PGF2 alpha 1.8 ng/g, compared to 57.5 ng/g in untreated and 1.4 ng/g in nonlesioned animals). The results suggest that some components of the prostaglandin system are involved in mechanisms underlying a widespread depression in functional state of the rat brain that develops in response to injury. In control animals, indomethacin was shown to have a biphasic effect on LCBF, an early depression shown previously by others followed at 24 h by a considerable increase.

Action of angiotensin on vascular and intestinal smooth muscle and its antagonism by saralasin

Angiotensin II was tested for its activity on rabbit aorta, lower esophageal sphincter (LES) from the rat, rat gastric fundus and rat colon. The peptide had a powerful stimulatory effect on vascular and extravascular smooth muscle beginning from concentrations of 10(-10) M. Its effect was antagonized by saralasin which acted in the different preparations to approximately the same extent: active concentrations of saralasin varied from 10(-8) M to 10(-7) M. The activity of angiotensin on the rabbit aorta appeared to be a direct one on its specific receptors. A mixed action connected with stimulation of adrenergic alpha receptors was observed in the rat LES, whereas an interference of the prostaglandin system was pointed out in the rat fundus and the rat colon. The circumstance of a similar sensitivity of the various tissues to the stimulatory effect of angiotensin and a similar degree of antagonism induced by saralasin tends to minimize the hypothesis of different subtypes of angiotensin receptors at least under the conditions of the present investigation.

Inhibition of prostaglandin synthesis by indomethacin does not affect alcohol consumption in inbred mice.

The prostaglandin system has been implicated in mediating both the acute and chronic pharmacologic effects of alcohol. The effect of blockade of prostaglandin synthesis by indomethacin on genetically based alcohol preference in C57BL/6, C3H/He, and BALB/c mice was examined. Although strain typical alcohol preference patterns were observed, there was no effect of indomethacin on either naive or preestablished alcohol preference and consumption. Genetically transmitted alcohol preference may be a complex system in which prostaglandin synthesis does not play a part.

Urinary prostaglandin E2 and kallikrein excretion in glucocorticoid hypertension in rats.

1. Oral administration of dexamethasone (about 2.5 X 10(-7) mol/day) caused hypertension in rats. The blood pressure rose from 108 +/- 6 (mean +/- SD) to 156 +/- 17 mmHg on the seventh day. The urine volume and urinary excretion of sodium were increased. The plasma renin activity and plasma aldosterone were unchanged. However, the urinary excretions of prostaglandin E2 (UPGE2V) and kallikrein (Ukall.V) were markedly decreased throughout the experiment. 2. With concurrent administration of captopril, the elevation of blood pressure was partially prevented. In this group of rats, the plasma renin activity was elevated and the reductions in UPGE2V and Ukall.V were partially prevented. 3. Based on these results, it is suggested that suppression of the kallikrein-kinin and prostaglandin systems, in addition to involvement of the renin-angiotensin system, is one of the factors contributing to the hypertensive action of dexamethasone.

Furosemide fails to alter plasma active or inactive renin in conscious sheep but does so in anaesthetized animals.

Regulation of plasma levels of active and inactive renin was investigated using sheep with indwelling artery, vein and bladder catheters. Control and experimental studies were carried out in the same animals on different days. Volume depletion during any single experiment was limited to a maximum of 50 ml. Despite large changes in sodium and water excretion, the diuretic furosemide at two dose levels, 1 and 10 mg/kg, failed to alter plasma levels of either active or inactive renin in conscious sheep. Induction of pentobarbitone anaesthesia in the sheep did not, per se, alter either plasma active or inactive renin. Furosemide (10 mg/kg) in anaesthetized animals produced a similar diuresis and natriuresis response to conscious sheep, but plasma active renin increased by 270% and inactive renin decreased to zero. In conscious sheep given an infusion of papaverine, furosemide also produced an increase in plasma active renin and a concurrent decrease in the inactive form. In both anaesthetized animals and in conscious sheep infused with papaverine, furosemide-induced intrarenal vasodilation, as evidenced by changes in clearance of p-aminohippuric acid, was much reduced in comparison to the conscious animals. This may be significant in relation to the control of renin secretion. It appears that the macula densa sodium receptor, which is considered to regulate renin release, will only function after it has been primed by other intra- or extrarenal factors. This is discussed, particularly in relation to the possible role played by the prostaglandin system.

Dietary potassium and the development of hypertension in two-kidney, one clip Goldblatt hypertensive rats.

HomeHypertensionVol. 5, No. 4Dietary potassium and the development of hypertension in two-kidney, one clip Goldblatt hypertensive rats. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessAbstractPDF/EPUBDietary potassium and the development of hypertension in two-kidney, one clip Goldblatt hypertensive rats. J Treasure, J Work, C Palmer and D Ploth J TreasureJ Treasure Search for more papers by this author , J WorkJ Work Search for more papers by this author , C PalmerC Palmer Search for more papers by this author and D PlothD Ploth Search for more papers by this author Originally published1 Jul 1983https://doi.org/10.1161/01.HYP.5.4.521Hypertension. 1983;5:521–528 Previous Back to top Next FiguresReferencesRelatedDetailsCited By Ishimitsu T, Tobian L, Uehara Y, Sugimoto K and Lange J (1995) Effect of high potassium diets on the vascular and renal prostaglandin system in stroke-prone spontaneously hypertensive rats, Prostaglandins, Leukotrienes and Essential Fatty Acids, 10.1016/0952-3278(95)90124-8, 53:4, (255-260), Online publication date: 1-Oct-1995. Liu D, Wang M, Kincaid-Smith P and Whitworth J (2009) The Effects of Dietary Potassium on Vascular and Glomerular Lesions in Hypertensive Rats, Clinical and Experimental Hypertension, 10.3109/10641969409067953, 16:4, (391-414), Online publication date: 1-Jan-1994. Linas P (1991) The role of potassium in the pathogenesis and treatment of hypertension, Kidney International, 10.1038/ki.1991.95, 39:4, (771-786), Online publication date: 1-Apr-1991. Mills E, Coghlan J, Denton D, Spence C, Whitworth J and Scoggins B (2009) The Anti-Hypertensive Effect of Potassium Loading in Experimental Hypertension: A Comparison of Sheep with Other Species, Clinical and Experimental Hypertension. Part A: Theory and Practice, 10.3109/10641968809103528, 10:2, (289-309), Online publication date: 1-Jan-1988. Treasure J and Ploth D (1983) Role of dietary potassium in the treatment of hypertension., Hypertension, 5:6, (864-872), Online publication date: 1-Nov-1983. July 1983Vol 5, Issue 4 Advertisement Article InformationMetrics Copyright © 1983 by American Heart Associationhttps://doi.org/10.1161/01.HYP.5.4.521PMID: 6345361 Originally publishedJuly 1, 1983 PDF download Advertisement

Prostaglandins and prostaglandin inhibitors in ischemic heart disease.

The evidence for a role of the prostaglandin system in myocardial ischemia and its consequences is still fragmentary. We review the factors that alter the relation between thromboxane A2 and prostacyclin production such that vasoconstriction, platelet aggregation, and the tendency toward thrombus formation are increased. Strategies to prevent platelet aggregation by interfering with the production of thromboxane A2 or by stimulation or administration of prostacyclin are currently under investigation in a number of centers. The ubiquity of the prostaglandin system and our incomplete understanding make careful long-term clinical trials and observations essential if we are to be sure that the net effect of these attempts is beneficial.