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Diabetes And Hypertension-Common Soil Hypothesis 37
How are Diabetes and Hypertension coined to point out that the two diseases originate
Related? from the same soil rooting from insulin resistance.
Diabetes and hypertension are considered to be “co- The insulin resistance and the resultant hyperinsu-
morbidities” which tend to occur together because linemia,affectnitric oxide pathway, activates sympa-
they share certain physiological traits. thetic drive, increases in vascular smooth muscle
cell (VSMC) cytosolic calcium, induction of endo-
These two diseases sharethe important risk factors thelin secretion, and enhancement of vascular lipid
like
deposition, sodium fluid retention, all contributing to
• Aging the pathogenesis of hypertension. Effect of insulin
on the blood vessel cells stimulates the proliferation
• Body Mass – overweight and obesity
of VSMCs by increasing insulin like growth factor 1
• Diet – High fat diets, rich in salt and processed (IGF 1) expression and also stimulates endogenous
sugars angiotensinogen and angiotensin II expression and
upregulation of angiotensin 1 receptors.The smooth
• Low physical activity
muscle cell migration and proliferation occurred
• Dyslipidemia bypotentiation of mitogenesis through Epidermal
Growth Factor/Platelet Derived Growth Factor recep-
• Atherosclerosis
tor (EGF/PDGF).Hyperinsulinemia stimulates the ex-
Types of Hypertension in Diabetes Mellitus pression of endothelin 1, a potent mitogen for VSMCs.
Insulin resistance prevents intracellular magnesium
1. Hypertension associated with type 2 DM (Syn- transport into VSMCs and diminishes Na/K ATPase
drome X) activity resulting in elevated cytosolic calcium and
2. Hypertension associated with nephropathy in increased vascular tone.
type 1 DM Hyperglycemia also has a direct effect onthe Renin-
3. Coincidental hypertension in diabetic patients Angiotensin Aldosterone System (RAAS).
- Essential hypertension Activation of the RAAS results in unregulated an-
- Isolated systolic hypertension giotensinogen II activity through its angiotensin 1 re-
- Renal scarring from recurrent pyelonephritis ceptor leading to the formation of Reactive Oxygen
4. Diabetogenic anti-hypertensive drugs Species (ROS). RAAS activation also leads to uninhib-
- Potassium-losing diuretics (chlorthali- ited production of aldosterone, which in turn induces
done,high dose thiazides) salt retention, enhanced sympathetic and decreased
- High dose beta blockers parasympathetic activity and increased extracellular
- Combination ofdiureticsand beta blockers matrix deposition.
5. Drugs causing hypertension and glucose intol- Hyperglycemia has mitogenic and antiapoptotic ef-
erance fects on VSMCs. It has the direct suppressive effect
- Corticosteroids on nitric oxide release and inturn reduces vasodila-
- Combined oral contraceptive pills tion effect. Glucose activates the nuclear transcrip-
tion factor (NFκB) through a Protein Kinase C (PKC)
6. Endocrine disorders causing hypertension and dependent pathway and upregulates Plasminogen
glucose intolerance Activator Inhibitor (PAI 1) expression and angiotensin
- Acromegaly II mediated action.Increased oxidative stress and re-
- Cushing’s syndrome duced prostacyclin synthase activity compromises
- Conn’s syndrome vasodilatation. The Advanced Glycation Endproducts
- Pheochromocytoma (AGEs) in circulation and vessel wall are associated
with impaired endothelial dependent vasodilatation
The Pathophysiology 2,4 and increased vessel wall stiffness.
Thecommon pathophysiological mechanism contrib- Increased sympathetic activity has been observed in
utes to both occurrences as well as exacerbation of people with insulin resistance and obesity.
these two conditions.
High serum leptin levels (hyperleptinemia)from the
The insulin resistance hypothesis is gaining more increased fat mass or secondary to leptin receptor re-
acceptance as a common etiological factor for both sistance are further potentiated by hyperinsulinemia.
diseases; “the common soil hypothesis” is a term
Cardio Diabetes Medicine

