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Am J Physiol. 1986 Jun;250(6 Pt 2):F980-5.
Prostaglandin E2 but not I2 restores furosemide response in indomethacin-treated rats.

Kirchner KA, Martin CJ, Bower JD.

Indomethacin attenuates furosemide's natriuretic response. Although this has been attributed to cyclooxygenase inhibition, attempts to correlate prostaglandin (PG) production with furosemide's natriuresis have led some investigators to conclude that prostaglandins are not involved in this response. This study was designed to evaluate the effects of intraaortic administration of PGE2, PGI2 (100 ng X kg-1 X min-1), or the vasodilators secretin or bradykinin (75 microU X kg-1 X min-1) on the furosemide-indomethacin antagonism. Fractional sodium excretion (FENa) during furosemide administration was 4.59 +/- 0.50% in control rats but 1.84 +/- 0.33% in indomethacin-treated rats (Indo) (P less than 0.001). PGE2 prevented indomethacin from attenuating furosemide's response (FENa, 3.91 +/- 0.25%; P = NS vs. control; P less than 0.01 vs. Indo). PGI2, however, failed to prevent the furosemide-indomethacin antagonism (FeNa, 1.94 +/- 0.59%, P less than 0.001 vs. control; P = NS vs. Indo). Inulin clearance, arterial pressure, filtered sodium load, and renal blood flow were not different between groups. Neither secretin nor bradykinin prevented the indomethacin-furosemide antagonism. This study is consistent with the hypothesis that indomethacin antagonizes furosemide's natriuretic response by prostaglandin synthesis inhibition. Furthermore, PGE2 seems to restore furosemide's response through actions other than a vasodilatory effect.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3521327&dopt=Abstract




Adv Exp Med Biol. 1986;198 Pt A:279-82.
Effect of furosemide on the rat submandibular gland kallikrein secretion.

Catanzaro OL, Vila SB, Zuccolo A, Seeber AM.

The effects of furosemide and Captopril were studied in normals and nephrectomized rats. Different doses of furosemide (5 to 50 mg/kg) increased the saliva kallikrein activity of submaxillary gland perfused with pilocarpine. Rats injected with captopril (10 mg) increased the blood flow of the gland, but did not modify the blood pressure. After furosemide (50 mg/kg) and captopril (10 mg), a decrease in arterial blood pressure was observed. The results suggest a release of glandular kallikrein which is secreted from the gland directly into the vascular compartment. On the other hand, rats sialodectomized showed no alterations in blood pressure in response to both drugs. These data suggest that submaxillary gland kallikrein play a role in regulating blood flow of the gland and blood pressure, at least in our experimental conditions.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3544715&dopt=Abstract




Hypertension. 1985 May-Jun;7(3 Pt 2):I49-54.
Role of the macula densa in renin release.

Itoh S, Carretero OA.

To examine the role of the macula densa in renin release, afferent arterioles alone or afferent arterioles with the macula densa attached were microdissected from rabbit kidney and incubated in Medium 199 for two consecutive 30-minute periods. Renin concentration in the medium was measured using partially purified rabbit angiotensinogen. Renin release rate over 1 hour from a single arteriole (or an arteriole with macula densa) was calculated and expressed as nanograms of angiotensin I generated per hour per arteriole (or arteriole with macula densa) per hour incubation (ng of ANG I X hr-1 X Af-1/hour). Basal renin release rate from afferent arterioles was 0.69 +/- 0.13 ng of ANG I X hr-1 X Af-1/hour (mean +/- SEM, n = 9) and remained stable for 60 minutes. Basal renin release rate from arterioles with macula densa was 0.25 +/- 0.03 ng of ANG I X hr-1 X Af + MD-1/hour (n = 9), which was significantly lower (p less than 0.025) than that from afferent arterioles alone. When furosemide (1.5 X 10(-3) M) was added to afferent arterioles alone, no significant change in renin release was observed (percent change from control; 24.8 +/- 29.9%; p greater than 0.05, n = 6). When furosemide was added to arterioles with macula densa attached, however, renin release increased by 387 +/- 46% (n = 7; p less than 0.001). After pretreatment with indomethacin, a cyclooxygenase inhibitor, furosemide still increased renin release from 0.17 +/- 0.03 to 0.60 +/- 0.10 ng of ANG I X hr-1 X Af + MD-1/hour (n = 4; p less than 0.05); however, indomethacin pretreatment reduced both the basal renin release rate and the absolute change in renin release induced by furosemide. We conclude that (1) the macula densa inhibits renin release in this preparation, (2) the macula densa plays a central role in furosemide-induced renin release, and (3) while the prostaglandin system is not essential for furosemide-induced renin release, it may be a modulating factor.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3888838&dopt=Abstract












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