Cardiac and liver function modulation effects of nanosilver in salt-induced hypertensive Sprague Dawley rats

  • O.K. Uche
  • E Ogbomwan


Aim: This study examined the effects of Nanosilver solution (10 ppm) (NAgs) on histopathology of myocytes, cardiac biomarker enzyme-creatine kinase muscle (CK-MB) and some liver function enzymes on salt-induced hypertensive sprague-dawley rats (SHRs).

Methods: Twenty four male rats (inbred) (90-120g) randomly grouped into 4 (n=6) respectively after acclimatization. Group 1(control) received normal rat chow + fresh tap water. Group 2 received rat chow containing 8% NaCl (high salt diet-HSD). Group 3 received [rat chow + NAgs (0.18ml) 10ppm/kg /day)].While group 4 received HSD + NAgs by oral gavage for 6 weeks. Blood pressure (BP) mmHg and heart rate (HR) bpm were measured using blood pressure transducer by cannulation of the left common carotid artery following anaesthesia with urethane. 5ml of blood was collected to assay for some liver enzymes (ALT, AST and ALP). Cardiac homogenate and tissue were prepared for CK-MB and histological studies.

Result: CK-MB level was significantly elevated in the SHRs and NAgs co-treated group compared with the control and NAgs-treated normotensive rats (NRs). Histomyograph of SHRs and cotreated NAgs showed varied histological distortion of the coronary vessels, ulceration, vascular dilatation, focal degeneration and asymmetrical medial hypertrophy. AST and ALP levels were, significantly (p<0.05) higher in SHRs, markedly increased in SHRs cotreated NAgs and NAgs-treated NRs compared with the control. ALT level showed a similar trend but with marked elevations in NAgs treated NRs compared with the control and SHRs.

Conclusion: Nanosilver solution and salt-induced hypertension synergistically may induce hepatotoxicity and are capable of causing structural distortions in cardiac myocytes.

Keywords: Salt-induced hypertension, Nanosilver, CK-MB and Liver enzymes

Short running title: Modulation effects of Nanosilver solution in hypertension


Journal Identifiers

eISSN: 1596-6569