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Curr Trend Cardiol. 2017 | Volume 1 Issue 3
September 18-19, 2017 | Toronto, Canada
Annual Conference on
HEART DISEASES
Diabetes has been implicated as a major risk factor in the
development of cardiovascular and renal complications.
Previous studies have indicated altered activities of the
bradykinin-forming components in diabetic patients as well
as diabetic experimental animals. Type2 diabetes can lead
to hypertension, renal and cardiac complications resulting
in high rates of mortality worldwide and in Kuwait as well.
Bradykinin (BK), a pharmacologically active polypeptide, is
one of kinins which is released in the tissues and body fluids
as a result of enzymatic action of kallikreins on kininogens.
The two types of kallikreins are tissue kallikrein and plasma
kallikrein. Tissue kallikrein is mainly expressed in the kidney
(urine), glandular tissue, vasculature, heart and brain. It
preferentially acts on low molecular weight kininogen
substrate to release lysyl-BK. Tissue kallikrein has also been
reported to be present in plasma . Plasma kallikrein acts on
high molecular weight kininogen substrate to release BK.
BK promotes both cardiovascular and renal functions, for
example, vasodilation, naturesis and diuresis (7,8). BK is
rapidly (< 15 sec) inactivated by circulating kinases (9). BK
acts on B1receptors and B2 receptors to elicit physiological
and pharmacological actions. It has been shown previously
that type 1 diabetic patients are at a risk of developing
nephropathy.
In addition, BK has been implicated in the pathophysiology
of hypertension. In this regard, it is suggested that the role
of renal BK is to excrete the excess of sodium. Therefore, a
reduction in the generation of renal BK may be the cause
in the development of hypertension as a result of the
accumulation of sodium in the body. Thus, the development
of a compound having renal kallikrein-like activity may
serve the purpose of excreting excessive sodium from the
kidney in the treatment of hypertension. Transgenic mice
over-expressing renal tissue kallikrein were hypotensive and
that administration of aprotinin, a tissue kallikrein inhibitor,
restored the BP of the transgenic mice. Recently, it has been
proposed that tissue kallikrein gene delivery into various
hypertensive models exhibits protection, such as reduction
in high blood pressure, attenuation of cardiac hypertrophy,
inhibition of renal damage and stenosis. This may indicate the
future therapeutics aspect of tissue kallikrein gene therapy
for hypertension, cardiovascular and renal pathology.
Abnormal BK and nitric oxide levels have been demonstrated
in diabetic patients in our study.
Speaker Biography
Jagdish N. Sharma is currently a Professor in the Department of Pharmacology and
Therapeutics of which he is the Founding Chairman, Faculty of Pharmacy, Kuwait
University, Kuwait. He has also served as a Professor of Pharmacology at the Universiti
Sains Malaysia, Penang, Malaysia, prior to joining Kuwait University in 1999. Prof.
Sharma received his . & A.H. (D.V.M.) in 1970 from Jawaharlal Nehru Agricultural
University, Jabalpur, India; his . in Medical Pharmacology in 1973 from the All-
India Institute of Medical Sciences, New Delhi, India; and his Ph.D. in Pharmacology
in1976 from the University of Strathclyde, Glasgow, Scotland, UK. The Calamus
International University, London in 2011, awarded degree in Health Sciences to
Professor Sharma in recognition of his outstanding highly accomplished professional
achievements in research and academic contributions. In 1995, he was elected to an
F.C.P. (Fellow) from the American College of Clinical Pharmacology, New York, USA and
an F.I.Biol. (Fellow) in 1997 from the Royal Institute of Biology, London, UK. This is
a highly prestigious award considered to be at the level of British DSc. Prof. Sharma
is an author of a book entitled “Topics in Mediators Pharmacology”, which has been
published by the Nova Science Publishers Inc., N.Y., USA. Prof. Sharma is the Editor
of a book Progress in Drug Research” series entitled “Recent Developments in the
Regulation of Kinins” 2014 which is published by Springer Basel AG, Switzerland. He
has been to numerous International conferences as invited speaker. Prof. Sharma has
been holding several research grants for the support of his clinical and basic research
activities and supervised PhD and MSc theses. He has been PhD external examiner and
evaluator for promotions to the ranks of Associate Professor and Professor externally.
In Malaysia, his research investigations were funded by the Ministry of Science and
Technology, Malaysia. Currently his clinical priority research grant is funded by the
Kuwait University research sector. He is the editorial board member of Pharmacy
Times (USA) of Middle East from 2007 to date, Inflammopharmacology (UK) from 1997
to date, International Journal of Immunopathology and Pharmacology (Italy) from
2006 to date, European Journal of Inflammation (Italy) from 2006 to date, Archives of
Medical Research (Mexico City) from 2006 to date, Clinical Medicine: Endocrinology
and Diabetes (New Zealand) from 2008 to date, Clinical Medicine: Therapeutics (New
Zealand) from 2009 to date, American Journal of Biomedical Sciences (USA) from 2009
to date and Journal of Pharmaceutical Technology and Drug Research (UK) from 2011
to date. He has 110 publications in reputed international biomedical journals, and
65 abstracts of national and international conferences. His work is supported by the
Kuwait University Grant RP01/09.
e:
Recent developments in the kallikrein-kinin system with hypertension and diabetes
Jagdish N Sharma
Kuwait University, Kuwait