Uncontrolled hypertension, uncompensated type II diabetes, and smoking have different patterns of vascular dysfunction.
OBJECTIVE
We evaluated the vascular reactivity in healthy subjects, heavy smokers, uncompensated type II diabetics, and patients with uncontrolled essential hypertension. Plasma nitrite/nitrate, cyclic 3',5'-guanosine monophosphate (cGMP), and thromboxane (TX)-B(2) levels were measured.


METHODS
One hundred participants were classified into four groups: normal control subjects (n = 25), heavy smokers (n = 25), uncompensated type II diabetics (n = 25), and patients with uncontrolled essential hypertension (n = 25).


METHODS
The brachial artery diameter was measured by a high-resolution ultrasound technique before and after reactive hyperemia and glyceryl trinitrate (GTN), 0.4 mg, administration. Plasma nitrite/nitrate, cGMP, and TX-B(2) levels were also measured.


RESULTS
Heavy smokers, uncompensated type II diabetics, and uncontrolled hypertensive patients showed impaired endothelium-dependent, nitric oxide (NO) flow-mediated vasodilatation (8.0 +/- 2.5%, 5.8 +/- 2.7%, and 7.2 +/- 3.3%, respectively [mean +/- SD]) when compared to the control subjects (12.6 +/- 3.6%; p < 0.01). Smokers had a normal endothelium-independent function induced by NO donor (GTN) [25.0 +/- 7.3% vs 25.3 +/- 8.5% for control subjects]. Uncompensated type II diabetics and patients with uncontrolled hypertension had impaired endothelium-independent responses (17.7 +/- 7.1% and 16.8 +/- 6.9%, respectively, vs 25.3 +/- 8.5 for normal control subjects; p < 0.05). Plasma levels of cGMP and TX-B(2) were not significantly different in the four groups, but nitrite/nitrate concentrations were increased in diabetics compared to the control subjects (266 +/- 47 micro mol/L vs 98 +/- 18 micro mol/L, p < 0.05).


CONCLUSIONS
Both uncontrolled hypertension and type II diabetes mellitus, but not smoking, are associated with impaired vascular smooth-muscle reactivity induced by NO donors. However, only uncompensated type II diabetics showed an increase in plasma nitrite/nitrate levels, suggesting an association with excessive production and/or inactivation of NO.
Yugar-Toledo
Juan Carlos
JC
Department of Pharmacology, Cardiovascular Pharmacology Laboratory, Faculty of Medical Sciences, State University of Campinas, Unicamp, Campinas, SP, Brazil.
Tanus-Santos
Jose Eduardo
JE
Sabha
Maricene
M
Sousa
Márcio Gonçalves
MG
Cittadino
Máira
M
Tácito
Lúcia Helena Buonalumi
LH
Moreno
Heitor
H
D000328:Adult; D001783:Blood Flow Velocity; D006152:Cyclic GMP / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology; D006801:Humans; D006940:Hyperemia; D006973:Hypertension / Q000097:blood / Q000503:physiopathology*; D008875:Middle Aged; D009566:Nitrates / Q000097:blood; D009569:Nitric Oxide / Q000096:biosynthesis / Q000502:physiology; D009573:Nitrites / Q000097:blood; D005996:Nitroglycerin / Q000494:pharmacology; D012907:Smoking / Q000097:blood / Q000503:physiopathology*; D013929:Thromboxane B2 / Q000097:blood; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
D009566:Nitrates; D009573:Nitrites; D014665:Vasodilator Agents; D009569:Nitric Oxide; D013929:Thromboxane B2; D005996:Nitroglycerin; D006152:Cyclic GMP