156 Chapter 6
Figure 6.31 The G-protein cycle. (1) When the receptor is not bound to the regulatory molecule, the three G-protein subunits
are aggregated together with the receptor, and the a subunit binds GDP. (2) When the regulatory molecule attaches to its receptor, the
a subunit releases GDP and binds GTP; this allows the a subunit to dissociate from the b g subunits. (3) Either the a subunit or the b g
complex moves through the membrane and binds to the effector protein (an enzyme or ion channel). (4) The a subunit splits GTP into
GDP and P i , causing the a and b g subunits to reaggregate and bind to the unstimulated receptor once more.
EffectorsUnstimulated
stateActivated
stateEffectorsGTPGTP
GDPGTP
GDP12(^33)
4
4
Regulatory molecule
Nucleotide Receptor
exchange
- Pi
α
α
α
α
β
β
β
β
γ
γ
γ
γ
| CHECKPOINTS
- Distinguish between synaptic, endocrine, and
paracrine regulation. - Identify the location of the receptor proteins for
different regulatory molecules.
Jessica’s hyperglycemia caused her renal carrier proteins
to become saturated, resulting in glycosuria (glucose in
the urine). The elimination of glucose in the urine and its
consequent osmotic effects caused the urinary excretion
of an excessive amount of water, resulting in dehydra-
tion. The diuretic she was taking for her hypertension
may have exacerbated this dehydration. Dehydration
raised her plasma osmolality, stimulating the thirst cen-
ter in the hypothalamus. (Hyperglycemia and excessive
thirst and urination are cardinal signs of diabetes mel-
litus.). Dehydration raises plasma solute concentrations,
but her plasma K^1 concentration decreased because
the diuretic caused urinary loss of K^1. This hypokalemia
affected her cardiac resting membrane potential and pro-
duced ECG abnormalities.
See the additional chapter 6 Clinical Investigation on
Recessive Genetic Kidney Disorder in the Connect site for
this text.