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Biomedical subjects

J N Sharma

Publications and source records attributed to J N Sharma.

At least 55 records · Page 3Linked to original sources
PubMed1986

A synovial amidase acting on tissue kallikrein-selective substrate in clinical and experimental arthritis.

Increased levels of amidase acting on a tissue-kallikrein selective substrate, Val.Leu.Arg.pNA, with an activity optimum at pH9, were detected in blood-free inflamed tissues from adjuvant arthritic rats (p less than 0.01). The component of this activity resistant to inhibition by soybean trypsin inhibitor (SBTI) also greatly increased (p less than 0.05). Both the SBTI-sensitive and SBTI-resistant components were inhibited by aprotinin (93% and 72% respectively). Kallikrein-like amidase also increased in inflamed synovia from seropositive rheumatoid, and osteoarthritic dogs when compared with healthy canine synovia. This increase was parallelled by an increase in kinin-forming enzyme which was also measured in rheumatoid and healthy animals and this activity was inhibited 72% by aprotinin. Total kallikrein-like amidase also increased 989% (p less than 0.05) in synovia from seropositive rheumatoid human patients, compared with healthy synovial tissue. Evidence is presented indicating that the origin of this enzymic activity may be plasma kallikrein.

Amidohydrolases↗
PubMed1984

The effect of indomethacin on the duration of the hypotensive action of bradykinin in Dahl salt-resistant rats: role of cyclooxygenase inhibition.

The Dahl salt resistant (DR) rat maintained on a low, 0.4%, or a high 8.0% salt-diet remained normotensive. The bradykinin (BK) induced falls in the systolic (SBP) and diastolic (DBP) were unaffected (P greater than 0.05) by the presence of indomethacin (5 mg/kg). Indomethacin, however, caused a substantial (P less than 0.001) reduction in the duration of the hypotensive action of bradykinin. It is speculated that the indomethacin effects result from an inhibition of the cyclooxygenase system in DR rats.

Animals↗
PubMed1984

Differential sensitivity of Dahl salt-sensitive and Dahl salt-resistant rats to the hypotensive action of acute nifedipine administration.

The calcium antagonist, nifedipine, was intravenously administered in a cumulative fashion, from 0.5 to 12 mg/kg, to Dahl salt-sensitive (DS) and Dahl salt-resistant (DR) rats which had been maintained on a high (8.0%) or low (0.4%) salt (NaCl) diet. We observed, compared with the DR rats, dose-related and significant (P less than 0.001) falls in the systolic (SBP) (72 +/- 3 and 60 +/- 9%, respectively) and diastolic blood pressure (DBP) (67 +/- 2 and 62 +/- 6%) o the DS rats maintained either on the low (0.4%) or high (8.0%) salt diets. In contrast, nifedipine therapy comparatively produced only moderate changes in the SBP and DBP of the DR rats (36 +/- 12, 27 +/- 9, 31 +/- 10, and 30 +/- 11%, respectively). We hypothesize that this differential sensitivity of the DS and DR rats to the hypotensive action of nifedipine may reflect a significantly more important role for a high resting Ca2+ influx, through nifedipine sensitive channels, in the maintenance of the blood pressure of the DS rat.

Animals↗
PubMed1984

Systolic blood pressure responses to enalapril maleate (MK 421, an angiotensin converting enzyme inhibitor) and hydrochlorothiazide in conscious Dahl salt-sensitive and salt-resistant rats.

Systolic blood pressure responses to enalapril maleate (MK 421, a new angiotensin converting enzyme inhibitor (CEI] and hydrochlorothiazide (HTZ) were studied in conscious Dahl salt-sensitive (DS) and salt-resistant (DR) rats maintained on a high salt (8.0% NaCl) and a normal salt (0.4% NaCl) diet. The DS rats were severely hypertensive after 3 weeks on the high salt diet whereas the systolic blood pressure (SBP) of the DR rats were normotensive. Oral treatment with enalapril (15-100 mg X kg-1 X day-1) and HTZ (60-400 mg X kg-1 X day-1) caused a significant reduction of SBP in the DS rats with the high salt diet (P less than 0.001); however, this was not observed until after 4 weeks of treatment when the dosage was 30 and 150 mg X kg-1 X day-1, respectively. Furthermore, enalapril therapy alone significantly reduced the SBP of all groups of rats regardless of diet or Dahl strain (P less than 0.001), but this was not observed until the end of the 7th week of therapy in DR rats on 8.0% NaCl and the end of the 3rd week of therapy for DR and DS rats on 0.4% NaCl. These results suggest that enalapril may lower SBP by mechanisms other than those related to an action as a CEI.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1983

Cardiac regression and blood pressure control in the Dahl rat treated with either enalapril maleate (MK 421, an angiotensin converting enzyme inhibitor) or hydrochlorothiazide.

Enalapril maleate (MK 421), and hydrochlorothiazide were used to evaluate the control of hypertension and reversal of myocardial hypertrophy in Dahl sensitive (DS) and Dahl resistant (DR) rats given either a high (8% NaCl) or a low salt (0.4% NaCl) diet. Groups of six-week-old male DS and DR rats were treated with enalapril (15-100 mg/kg/day) in drinking water for eight weeks. Additional comparable groups of DS and DR were also treated with hydrochlorothiazide (60-400 mg/kg/day). Systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR) and heart weight/body weight (Hwt/Bwt) ratio were determined. We observed significant reduction in Hwt/Bwt ratio (P less than 0.001) along with control of SBP and DBP in the DS given a high salt diet treated with either enalapril or hydrochlorothiazide. However, in the DR given a high salt diet, cardiac regression (Hwt/Bwt ratio, P less than 0.05), SBP and DBP (P less than 0.01) reduction were seen only with enalapril. Similarly, cardiac regression (Hwt/Bwt ratio, P less than 0.05) was observed along with reduction of SBP and DBP (P less than 0.001) in the DS given a low salt diet and DR given enalapril. These data indicate that enalapril reduced SBP and DBP in association with cardiac regression in hypertensive and normotensive rats. In contrast, hydrochlorothiazide only reduced SBP, DBP and caused cardiac reversal (Hwt/Bwt ratio) in DS placed on a high salt diet.

Animals↗