Asset Details
MbrlCatalogueTitleDetail
Do you wish to reserve the book?
Diabetic Nephropathy Is Markedly Enhanced in Mice Lacking the Bradykinin B2 Receptor
by
Jennette, J. Charles
, Smithies, Oliver
, Kakoki, Masao
, Takahashi, Nobuyuki
in
Albumins
/ Animals
/ Biological Sciences
/ Blacksmithing
/ Diabetes
/ Diabetes complications
/ Diabetic nephropathies
/ Diabetic Nephropathies - etiology
/ Diabetic Nephropathies - pathology
/ Genetic mutation
/ Kidney - pathology
/ Kidney - ultrastructure
/ Kidneys
/ Male
/ Mice
/ Mice, Inbred C57BL
/ Receptor, Bradykinin B2 - genetics
/ Receptor, Bradykinin B2 - physiology
/ Receptors
/ RNA, Messenger - analysis
/ Type 1 diabetes mellitus
2004
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
You are currently in the queue to collect this book. You will be notified once it is your turn to collect the book.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Diabetic Nephropathy Is Markedly Enhanced in Mice Lacking the Bradykinin B2 Receptor
by
Jennette, J. Charles
, Smithies, Oliver
, Kakoki, Masao
, Takahashi, Nobuyuki
in
Albumins
/ Animals
/ Biological Sciences
/ Blacksmithing
/ Diabetes
/ Diabetes complications
/ Diabetic nephropathies
/ Diabetic Nephropathies - etiology
/ Diabetic Nephropathies - pathology
/ Genetic mutation
/ Kidney - pathology
/ Kidney - ultrastructure
/ Kidneys
/ Male
/ Mice
/ Mice, Inbred C57BL
/ Receptor, Bradykinin B2 - genetics
/ Receptor, Bradykinin B2 - physiology
/ Receptors
/ RNA, Messenger - analysis
/ Type 1 diabetes mellitus
2004
Oops! Something went wrong.
While trying to remove the title from your shelf something went wrong :( Kindly try again later!
Do you wish to request the book?
Diabetic Nephropathy Is Markedly Enhanced in Mice Lacking the Bradykinin B2 Receptor
by
Jennette, J. Charles
, Smithies, Oliver
, Kakoki, Masao
, Takahashi, Nobuyuki
in
Albumins
/ Animals
/ Biological Sciences
/ Blacksmithing
/ Diabetes
/ Diabetes complications
/ Diabetic nephropathies
/ Diabetic Nephropathies - etiology
/ Diabetic Nephropathies - pathology
/ Genetic mutation
/ Kidney - pathology
/ Kidney - ultrastructure
/ Kidneys
/ Male
/ Mice
/ Mice, Inbred C57BL
/ Receptor, Bradykinin B2 - genetics
/ Receptor, Bradykinin B2 - physiology
/ Receptors
/ RNA, Messenger - analysis
/ Type 1 diabetes mellitus
2004
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Diabetic Nephropathy Is Markedly Enhanced in Mice Lacking the Bradykinin B2 Receptor
Journal Article
Diabetic Nephropathy Is Markedly Enhanced in Mice Lacking the Bradykinin B2 Receptor
2004
Request Book From Autostore
and Choose the Collection Method
Overview
Type I human diabetics and streptozotocin-induced diabetic mice with higher genetically determined levels of angiotensin-converting enzyme have an increased risk of developing nephropathy. However, previous experiments in mice and computer simulations indicate that modest increases in angiotensin-converting enzyme have minimal effects on blood pressure and angiotensin II levels, although bradykinin decreases significantly, inferring that bradykinin is critical for protecting the kidney in diabetics. Here, we confirm this inference by demonstrating that Akita diabetic mice lacking the bradykinin B2 receptor develop overt albuminuria, excreting the equivalent of >550 mg/day albumin in humans, which contrasts with the microalbuminuria (equivalent to <150 mg/day) seen in their simply diabetic littermates. The overt albuminuria is accompanied by a marked increase in glomerular mesangial sclerosis. The importance of bradykinin demonstrated here bears strongly on how current drugs reduce diabetic nephropathy and suggests that B2 receptor-specific agonists merit consideration in this context.
Publisher
National Academy of Sciences,National Acad Sciences
MBRLCatalogueRelatedBooks
Related Items
Related Items
This website uses cookies to ensure you get the best experience on our website.