Kaplan’s Clinical Hypertension Eleventh Edition

Preface vii
1 Hypertension in the Population at Large 1
2 Measurement of Blood Pressure 18
3 Primary Hypertension: Pathogenesis (with a Special Section
on Renal Denervation and Carotid Baroreceptor Pacing) 40
4 Primary Hypertension: Natural History and Evaluation 116
5 Management of Hypertension: Why, When, How Far 142
6 Treatment of Hypertension: Lifestyle Modifications 179
7 Treatment of Hypertension: Drug Therapy 198
8 Hypertensive Emergencies 263
9 Renal Parenchymal Hypertension 275
10 Renovascular Hypertension 297
11 Primary Aldosteronism 320
12 Pheochromocytoma (with a Preface About Incidental Adrenal
Masses) 341
13 Hypertension Induced by Cortisol or Deoxycorticosterone 364
14 Other Forms of Identifiable Hypertension 378
15 Hypertension with Pregnancy and the Pill 398
16 Hypertension in Childhood and Adolescence

Kaplan’s Clinical Hypertension Eleventh Edition

Chapter 3 • Primary Hypertension: Pathogenesis 77
Small Vessel Rarefaction and
Impaired Tissue Perfusion
Both experimental and human hypertension are commonly
accompanied by microvascular rarefaction—
reduced number or combined length of small vessels
in a given volume of tissue (Levy et al., 2008). ROS
can cause both constriction of precapillary vessels
with functional rarefaction (decreased capillary
recruitment during metabolic demand) and apoptosis
with anatomic rarefaction (vascular smooth much cell
death with vessel dropout).
Microvascular rarefaction involves reduced skin
capillary recruitment and reduced reactive hyperemia
in forearm and coronary circulations even in the
absence of coronary atherosclerosis (Levy et al.,
2008). Microvascular rarefaction/ischemia is an
attractive mechanism explaining the frequent coexistence
of hypertension and diabetes (in particular,
impaired insulin-mediated glucose uptake in skeletal
muscle) and for the accelerated target organ damage
in patients with both conditions. Also, insulin
increases muscle perfusion by phosphorylating eNOS,
which opens precapillary sphincters to increase capillary
surface area for diffusion of oxygen, nutrients,
glucose, and insulin into skeletal muscle (Barrett
et al., 2009); thus, defective eNOS regulation is
another putative microvascular mechanism linking
diabetes and hypertension.